bims-engexo Biomed News
on Engineered exosomes
Issue of 2026–02–15
sixty-four papers selected by
Ravindran Jaganathan, Universiti Kuala Lumpur



  1. Cell Tissue Bank. 2026 Feb 10. 27(1): 9
      Bone regeneration remains a major clinical challenge due to the limited healing capacity of large bone defects and the limitations of conventional grafting or cell-based therapies. Exosomes, nanosized extracellular vesicles secreted by diverse cell types, have emerged as promising cell-free mediators of osteogenesis, angiogenesis, and immune regulation. However, the therapeutic efficacy of native exosomes is constrained by low yield, rapid clearance, and limited targeting. Because effective bone regeneration is inherently multi-factorial-requiring biomechanical stability, vascularization, and an instructive ECM and cellular microenvironment-engineered exosomes should be regarded as enabling components within integrated regenerative systems rather than a standalone solution. Recent advances in engineered exosomes (EExos) have opened new frontiers in bone tissue regeneration by enabling precise design, biofunctionalization, and targeted delivery. Engineering strategies-ranging from genetic modification of donor cells to chemical conjugation, hybrid nanocarrier formation, and controlled cargo loading-have been employed to enhance the osteoinductive and osteoconductive potential of exosomes. Furthermore, incorporation of EExos into smart delivery systems, such as hydrogel scaffolds, 3D-printed matrices, and bone-targeting ligands, offers sustained release and localized therapeutic effects within the bone microenvironment. This review comprehensively summarizes the latest developments in the design, delivery, and functional optimization of EExos for bone regeneration. Mechanistic insights into their roles in promoting bone remodeling, angiogenesis, and immune modulation are discussed alongside current translational progress, manufacturing challenges, and regulatory considerations. Finally, emerging directions-such as AI-assisted exosome engineering, CRISPR-based programming, and bioprinting-integrated therapies-are highlighted as transformative pathways toward personalized and clinically translatable bone regenerative medicine.
    Keywords:  Bone regeneration; Engineered exosomes; Regenerative medicine; Targeted delivery
    DOI:  https://doi.org/10.1007/s10561-026-10213-7
  2. PLoS One. 2026 ;21(2): e0341056
      SEC61G is an oncogene in hepatocellular carcinoma (HCC), a common malignant tumor worldwide. MicroRNAs (miRNAs) regulation of oncogenes are available therapeutic strategies being investigated in HCC, but the effective miRNA delivery remains a challenge. Here, we investigated the potential therapeutic effects of miRNA-loaded engineered exosomes in patients with HCC. MiRNAs that could bind to SEC61G were screened using Targetscan, and were verified using HepG2 cells viability after transfecting miRNAs mimic. Five miRNAs binding to SEC61G,among which, miR-651-3p and miR-488-3p mimic significantly inhibited HepG2 cells viability (p < 0.05) and decreased SEC61G protein expression. Then, dual-luciferase reporter assay also confirmed SEC61G as a target of miR-488-3p in HCC. After that, miR-488-3p-loaded engineered exosomes (Exo-miR-488-3p) were isolated from the supernatant of 488-3p-overexpressed cells and identified via nanoparticle tracking analysis, transmission electron microscopy and western blot. In vitro experiments showed that exo-miR-488-3p significantly inhibited proliferation, colony formation, migration and invasion of HepG2 cells than corresponding negative control. In addition, Exo-miR-488-3p tended to induce HepG2 cells apoptosis, though this relationship was not statistically significant. In conclusion, exo-miR-488-3p inhibits the malignant cytological activities in HCC, a possible strategy in the treatment of HCC.
    DOI:  https://doi.org/10.1371/journal.pone.0341056
  3. FASEB J. 2026 Feb 28. 40(4): e71564
      Exosomes are naturally occurring nanovesicles present in a variety of bodily fluids that facilitate the transport of proteins and nucleic acids. Characterized by their low immunogenicity and high biocompatibility, exosomes can efficiently navigate through biological barriers. This review summarizes the applications of exosomes in disease diagnosis and treatment, emphasizing their roles as biomarkers for non-invasive detection, as well as engineered vehicles for drug delivery and vaccine development. Additionally, this review also discusses recent technological advancements in exosome engineering, including genetic modification techniques and chemical modifications aimed at optimizing targeted delivery systems and enhancing immunomodulation strategies. Notably, it highlights the significant potential of exosomes to transform non-invasive diagnostics while promoting the development of sophisticated therapeutic carriers.
    Keywords:  engineering strategies; exosome; non‐invasive diagnosis
    DOI:  https://doi.org/10.1096/fj.202504351R
  4. Crit Rev Ther Drug Carrier Syst. 2026 ;43(1): 1-55
      Exosomes, a type of extracellular vesicle (EV), have received much attention in recent years for their potential in drug delivery systems and therapeutic applications. These nano-sized vesicles, secreted by various plant and animal species, serve as natural carriers of bioactive compounds, including proteins, lipids, and RNA, facilitating intercellular communication between tissue and cells and influencing physiological processes. Stahl and group discovered exosomes from maturing mammalian reticulocytes (immature red blood cells) in 1983, followed by Johnstone and colleagues in 1987, who named them exosomes. Animal-derived exosomes are a popular choice for small-molecule drug delivery due to their biocompatibility and homing properties in various domains, including biology and medicine. After animal-derived exosomes, researchers focused on plant-based exosomes and found several good sources of exosomes from different fruits, vegetables, leaves, and other parts of plants that have different effects like anticancer, anti-inflammatory, antioxidants, and so on. Plant-derived exosomes are also used as carriers for different drugs to treat disease. This review examines the biological component, biogenesis of plant exosomes, their sources, and the methodologies employed for their isolation and purification. We also explore the evaluation techniques for characterizing their biological components, such as proteins and lipids. Furthermore, we discuss the applications of plant-derived exosomes in drug delivery, highlighting their application in different disorders with some research references, including biocompatibility, stability, and targeted delivery. Additionally, this review also addresses the challenges associated with plant-based exosomes in different stages of research including isolation and purification, standardization, optimization, drug loading, and so on. The goal of this in-depth review is to provide insight into the current status of research on exosomes derived from plants and the ways that they could advance in drug delivery systems.
    DOI:  https://doi.org/10.1615/CritRevTherDrugCarrierSyst.2025057676
  5. Bioact Mater. 2026 Jun;60 472-491
      Age-related osteoporosis arises from bone tissue with inadequate metabolic support for osteogenesis. We identified that DNA methylation-mediated suppression of glutathione synthetase (GSS) represents an upstream lesion limiting endogenous glutathione (GSH) synthesis and supply in aged bone, thereby constraining osteoblast differentiation. In turn, impaired GSH synthesis exacerbates oxidative stress levels and diminishes osteogenic capacity, and this metabolic bottleneck is independent of substrate availability: cysteine supplementation neither restored GSH synthesis flux in aged bone nor rescued its osteogenic deficits. To overcome this limitation, we developed an exosome-based GSH delivery platform using electroporation to efficiently load GSH. These exosomes are derived from CXCR4-enriched bone marrow mesenchymal stem cells (BMSCs), leveraging CXCR4-mediated homing to the bone marrow niche to enhance bone retention, stabilize GSH during loading and circulation, and elevate local GSH pools at osteogenic sites. In aged bone, this targeted system sustainably delivers GSH, alleviates oxidative stress, improves mitochondrial function, delays cellular senescence, and promotes osteogenesis. In summary, while DNA methylation acts upstream to constrain GSH synthesis in aging bone, therapeutically correcting the resultant metabolic deficit via bone-homing exosome-mediated GSH delivery restores osteogenic function and improves bone metabolism in aged individuals.
    Keywords:  Age-related-Osteoporosis; CXCR4; Engineered exosomes; Glutathione; Oxidative stress
    DOI:  https://doi.org/10.1016/j.bioactmat.2025.12.048
  6. Mol Ther. 2026 Feb 06. pii: S1525-0016(26)00089-4. [Epub ahead of print]
      Insufficient accumulation of lipid nanoparticles (LNPs)-encapsulated mRNA vaccines within antigen-presenting cells (APCs) remains a key barrier to eliciting potent immune responses. Genetically engineered extracellular vesicles (EVs) present a highly adaptable and precisely tunable platform for the efficient delivery of small molecules to specific types of cells. In this study, we exploited a pseudotyping-based approach to load both exosome and microvesicle membranes with ectodomain of LpqH (LpqH48-159) through engineering the vesicular stomatitis virus (VSV)-G protein. Our findings demonstrated that loading LpqH ectodomain onto surface of exosomes or microvesicles led to an increase in targeting macrophages compared with commercialized LNPs. Meanwhile, the LpqH48-159-tagged microvesicles (LpqH-MV) exhibit not only a higher efficiency in macrophage targeting but also greater mRNA encapsulation efficiency compared to LpqH48-159-tagged exosomes. In a vaccine-related application, compared to the LNPs, the LpqH-MV loaded with mRNA encoding the enterovirus 71 capsid protein (VP1) or severe acute respiratory coronavirus 2 (SARS-CoV-2) receptor-binding domain (RBD) elicited stronger humoral and adaptive immune responses against viral infection via intramuscular or inhalable immunization, respectively. Our study demonstrated that LpqH48-159-tagged microvesicles serve as a promising platform for mRNA vaccine delivery, enhancing APCs targeting capabilities and thereby providing robust immune protection.
    DOI:  https://doi.org/10.1016/j.ymthe.2026.02.002
  7. Inflammopharmacology. 2026 Feb 10.
      Non-healing wounds, such as diabetic foot ulcers, burns, and pressure injuries, represent a persistent clinical challenge, affecting an estimated 2-5% of the global population and accounting for annual healthcare costs exceeding USD 25 billion. Their failure to heal is driven by unresolved inflammation, inadequate vascularization, and progressive disorganization of extracellular matrix (ECM) architecture, which collectively disrupt the coordinated cascade of tissue regeneration. Mesenchymal stem cell (MSC)-derived exosomes have emerged as a potent cell-free therapeutic approach capable of addressing these pathological barriers through multi-level biological modulation of immune, vascular, and stromal compartments. Preclinical studies demonstrate that topical or injectable administration of MSC-derived exosomes accelerates wound closure by 25-60% within 10-14 days compared to controls. Immunomodulatory effects include promoting macrophage polarization from M1 to M2 phenotypes, with reported increases in M2/M1 ratios of 1.5-3.2-fold, mediated by exosomal miRNAs (e.g., miR-223, miR-181c) and proteins that suppress NF-κB signaling. Angiogenesis is markedly enhanced, with microvascular density rising by 30-70%, driven by the transfer of VEGF, miR-126, and miR-21 to endothelial cells, thereby boosting migration and tube formation. Fibroblast activity is similarly upregulated, resulting in 1.4-2.0-fold increases in collagen deposition and restoration of the MMP/TIMP balance, leading to improved tensile strength and ECM integrity. Integration of biomaterial-assisted delivery platforms, including thermosensitive hydrogels, collagen scaffolds, and microneedle arrays, extends exosome retention and functional bioavailability at the wound site by 2-5 times compared to free vesicles. While early clinical trials report safety and feasibility, challenges in large-scale GMP manufacturing, batch-to-batch consistency, and regulatory harmonization. Overcoming these translational barriers through advances in bioengineering, genetic modification, and smart delivery systems may enable the evolution of MSC-derived exosomes into standardized, next-generation therapeutics for chronic, non-healing wounds.
    Keywords:  Angiogenesis; Cell-free therapeutics; Extracellular matrix remodeling; Fibroblast; MSC-derived exosomes; Macrophage polarization; Non-healing wounds
    DOI:  https://doi.org/10.1007/s10787-025-02084-3
  8. Bioact Mater. 2026 Jun;60 510-526
      Intracerebral hemorrhage (ICH) carries high mortality and disability rates, driven not only by the initial bleeding but also by secondary neurotoxicity from blood derived components such as hemoglobin. An effective strategy during the subacute phase must therefore address both hematoma clearance and neuroinflammation. To achieve this dual action therapy, we engineered a novel nanoplatform (M2-exo@HI) by encapsulating a plasmid co-expressing haptoglobin (Hp) and interleukin-10 (IL-10) within M2 macrophage-derived exosomes. Leveraging the innate inflammatory homing of macrophage exosomes, M2 exo@HI delivers the HI plasmid to the ICH site, where it is primarily internalized by M1 microglia. The expressed Hp binds hemoglobin, reducing neurotoxicity and exert neuroprotective effects. Simultaneously, IL-10 polarizes M1 microglia to the neuroprotective M2 phenotype, thereby removing hematoma and alleviating neuroinflammation via anti-inflammatory cytokine production. Consequently, M2-exo@HI significantly reduced hematoma volume, improved long-term neurological function, and enhanced blood-brain barrier (BBB) repair. Transcriptome analysis further elucidated the genetic mechanisms underlying this synergistic effect. This work presents a promising co-delivery strategy for enhancing hemorrhagic stroke therapy.
    Keywords:  Drug delivery; Hematoma clearance; M2 macrophage-derived exosomes; Nanocarriers; Neuroinflammation alleviation
    DOI:  https://doi.org/10.1016/j.bioactmat.2026.01.047
  9. J Adv Res. 2026 Feb 11. pii: S2090-1232(26)00141-4. [Epub ahead of print]
       INTRODUCTION: Bone loss is associated with declines in immune function. Osteoblasts, as key regulators of bone formation and the bone marrow niche, may orchestrate this coupled deterioration, but the underlying molecular mechanisms require further elucidation.
    OBJECTIVES: This study aims to explore the molecular mechanisms by which functional degeneration of osteoblasts leads to immune decline in osteoporosis.
    METHODS: Immune cell populations in peripheral blood were analyzed in both osteoporotic patients and mice. USP26 expression was assessed in senescent osteoblasts and bones. Bone formation, B lymphopoiesis, and susceptibility to sepsis were evaluated in mice with osteoblast-specific conditional knockout of Usp26. A combination of transcriptomics, targeted metabolomics, and in vivo/in vitro experiments involving tryptophan metabolite supplementation and inhibition were performed to identify associated niche metabolic factors. Finally, the therapeutic potential of USP26 restoration was evaluated by administering USP26-modified, bone-targeting exosomes in osteoporotic and septic mouse models.
    RESULTS: In this study, we have identified the downregulation of USP26 in osteoblasts as a critical mechanism bridging bone loss and immune dysfunction. Mechanistically, the reduced USP26 levels impede osteoblast differentiation while facilitating the ubiquitin-mediated degradation of interleukin-4-induced protein 1 (IL4I1). This impairment collapses the tryptophan metabolic axis, specifically reducing the production of the endogenous tryptophan-derived indole metabolite, indole-3-acetic acid (IAA) and compromising B lymphopoiesis. Consistent with this, we observe the mice with USP26 deficiency in osteoblasts died earlier in sepsis conditions with decreased B cells. The bone-targeted delivery of USP26 in osteoporotic mice via engineered exosomes restored bone formation, rescued B cell production and improved infection resistance.
    CONCLUSION: Our findings establish osteoblastic USP26 as a dual regulator of bone formation and immune activation, indicating that modulating osteoblast function and targeting the USP26/IL4I1-AHR signaling axis may represent a promising therapeutic strategy for treating immune deficiency associated with age-related bone loss in clinical settings.
    Keywords:  B lymphopoiesis Niche; Bone target exosome; Interleukin-4-induced protein 1; Osteoblast; Ubiquitin specific protease 26
    DOI:  https://doi.org/10.1016/j.jare.2026.02.010
  10. Cells. 2026 Jan 30. pii: 264. [Epub ahead of print]15(3):
      Acute lung injury (ALI) is a clinically severe respiratory disorder, of which autophagy is the crucial mechanism. Exosomes have the potential to treat ALI, but the role of adipose-derived exosomes (ADEs) in the autophagy of ALI remains unclear. Using an LPS-induced ALI model, the effects of ADE isolated from a lean or diet-induced-obese (DIO) mouse and ADE-carried miRNAs were investigated. After administration of ADEs, the levels of autophagy-related molecules were determined by qRT-PCR, Western blotting, and immunohistochemical staining. Then, a miRNA targeting HMGB1 was screened by bioinformatic analysis and a dual-luciferase reporter assay, and its effect on the HMGB1-driven autophagy in an ALI mouse was investigated as ADEs. The data showed that LPS caused lung injury and activated HMGB1-driven autophagy. The ADEs from a lean mouse or DIO mouse significantly alleviated histopathological lesions, and they inhibited HMGB1-driven autophagy by down-regulating LC3, Beclin-1, and Atg5; the effects of ADEs were not significantly different between a lean and DIO mouse. Of the miRNAs carried by ADE, moreover, miR-142a-3p could specifically bind to HMGB1 mRNA, and up-regulation of pulmonary miR-142a-3p suppressed HMGB1-driven autophagy and relieved lung injuries. Our results indicated that miR-142a-3p and ADEs mitigate LPS-induced ALI by inhibiting HMGB1-driven autophagy, providing new insights on the prevention and treatment of ALI.
    Keywords:  acute lung injury; autophagy; exosome; miR-142a-3p
    DOI:  https://doi.org/10.3390/cells15030264
  11. bioRxiv. 2026 Feb 02. pii: 2025.10.07.681010. [Epub ahead of print]
      Engineered virus-like particles (eVLPs) are promising vehicles for transient delivery of gene editing agents. While extensive particle engineering has yielded efficient eVLPs, it remains underexplored whether engineering the cells used to produce eVLPs could further improve eVLP properties. We developed a genome-wide screening approach to systematically investigate how genetic perturbations in producer cells influence eVLP production. This approach generates eVLPs loaded with guide RNAs that identify the genetic perturbation in the cell that produced a particular particle; the abundance of each guide RNA in eVLPs therefore reflects how the corresponding genetic perturbation influences eVLP production or cargo loading. We applied this approach to identify several genes that regulate eVLP cargo expression and loading into particles during the production process. Leveraging these insights, we engineered producer cells that support increased eVLP cargo packaging and a 2- to 9-fold increase in eVLP delivery potency across several cargo, particle, and target-cell types in cultured cells and in mice. Our findings suggest the potential of producer-cell engineering as a useful strategy for improving the utility of eVLPs and related delivery methods.
    DOI:  https://doi.org/10.1101/2025.10.07.681010
  12. Respir Res. 2026 Feb 10.
       BACKGROUND: Acute lung injury (ALI) can initiate early epithelial remodeling that may precede pulmonary fibrosis, with EMT of alveolar epithelial cells implicated in this acute phase. While mesenchymal stromal cell (MSC)-derived exosomes exhibit repair potential, their conventional culture conditions fail to mimic the hypoxic microenvironment of ALI. Here, we explored the therapeutic effects and regulatory mechanisms of hypoxia-preconditioned bone marrow MSC-derived exosomes (HExos) in LPS-induced ALI with early epithelial remodeling.
    METHODS: BMSCs were characterized via osteogenic/adipogenic differentiation and flow cytometry. Exosomes derived under normoxia (NExos) and hypoxia (HExos) were isolated and validated using nanoparticle tracking analysis (NTA), transmission electron microscopy (TEM), and Western blot. An LPS-induced ALI mouse model was employed to evaluate exosome efficacy. Through integrated miRNA sequencing, luciferase reporter assays, and gain-/loss-of-function experiments, we examined a working model involving the miR-486a-5p/Skp2/GATA4 axis.
    RESULTS: HExos markedly alleviated LPS-induced acute lung injury and early-stage collagen deposition. Mechanistically, HExos were enriched with miR-486a-5p, which directly targeted Skp2, thereby reducing Skp2-mediated ubiquitin-proteasome degradation of GATA4 and attenuating EMT-like changes. Notably, miR-486a-5p mimics reversed EMT-like changes in alveolar epithelial cells, while its knockdown abolished the protective effect.
    CONCLUSIONS: Hypoxia-preconditioned bone marrow-derived mesenchymal stromal cell (BMSC) exosomes demonstrate significant potential to alleviate LPS-induced acute injury and early epithelial remodeling by engaging a miR-486a-5p/Skp2/GATA4 working model, offering a proof-of-concept therapeutic strategy for ALI.
    Keywords:  Acute lung injury; EMT; Exosomes; GATA4; Hypoxia; Skp2; miR-486a-5p
    DOI:  https://doi.org/10.1186/s12931-026-03560-2
  13. Sci Rep. 2026 Feb 07.
      This study aimed to investigate the role of miR-25-3p carried by human amnion epithelial cell (hAEC)-derived exosomes in regulating MUC5AC production and apoptosis in conjunctival goblet cells. hAEC-derived exosomes were isolated, characterized, and evaluated for their uptake by conjunctival goblet cells. qRT-PCR, flow cytometry, Western blotting, and ELISA were used to assess the effects of exosomes on MUC5AC expression and apoptosis, with a focus on the contribution of miR-25-3p. The interaction between miR-25-3p and its predicted target BCL2L11 was examined using dual-luciferase reporter assays. Conjunctival goblet cells efficiently internalized hAEC-derived exosomes. Exosome treatment increased MUC5AC expression (P < 0.01) and reduced apoptosis (P < 0.01). miR-25-3p was found to mediate these effects, at least in part, through targeting BCL2L11, thereby promoting MUC5AC production (P < 0.01) and decreasing apoptosis (P < 0.01). hAEC-derived exosomes, particularly those containing miR-25-3p, modulate mucin expression and apoptosis in conjunctival goblet cells. These findings provide mechanistic insight into how exosomal miRNAs may contribute to maintaining ocular surface homeostasis, suggesting a potential role for exosomal miR-25-3p in supporting ocular surface health.
    Keywords:  Conjunctival goblet cells; Exosomes; Human amnion epithelial cells; MUC5AC; miR-25-3p
    DOI:  https://doi.org/10.1038/s41598-026-37794-3
  14. J Nanobiotechnology. 2026 Feb 07.
      Exosomes serve as pivotal nanoscale messengers in intercellular communication by transporting bioactive molecules such as miRNAs, proteins, and lipids that regulate physiological and pathological processes. Emerging evidence highlights exercise as a potent modulator of exosome biogenesis, dynamically altering their release kinetics, molecular cargo, and bioactivity across tissues. Exercise-derived exosomes disseminate systemic adaptations by delivering regulatory signals to noncontractile organs, thereby coordinating multitissue responses that underlie the protective and reparative benefits of physical activity. This review synthesizes current knowledge on the dynamic effects of acute and chronic exercise on exosome profiles and their therapeutic potential in treating neurological, cardiovascular, metabolic, and musculoskeletal disorders. This review further discusses how exosome engineering and precision medicine could harness exosomes as "exercise mimetics," offering cell-free therapeutics for mobility-limited populations. By integrating exercise physiology with translational medicine, this work pioneers a new therapeutic paradigm where exosome-based molecular therapies replicate exercise's multisystem benefits.
    Keywords:  Disease; Exercise; Exosomes; Intercellular communication; Interorgan communication
    DOI:  https://doi.org/10.1186/s12951-026-04115-9
  15. Nanotechnology. 2026 Feb 09.
      Liver fibrosis represents a critical intermediate stage in the progression of chronic liver diseases toward cirrhosis. Conventional therapeutic strategies remain limited by insufficient efficacy, notable side effects, or narrow applicability, making the effective reversal of fibrosis a persistent clinical challenge. Although gene silencing technologies offer a promising therapeutic avenue, their clinical translation is hampered by poor delivery efficiency, instability in vivo, and lack of tissue specificity. To address these issues, we developed a lactobionic acid‑modified aminated glycogen (Lac‑AGly) nanoparticle system for the targeted delivery of connective tissue growth factor (CTGF) targeting siRNA. By utilizing natural glycogen as a biodegradable backbone, a degree of amination of 51.2% conferred efficient siRNA binding capacity, while lactobionic acid modification enabled selective recognition of hepatocyte-expressed asialoglycoprotein receptors (ASGPR). The resulting Lac-AGly/siCTGF nanocomplexes exhibited a uniform spherical morphology with an average particle size of 247.2 ± 8.8 nm and a zeta potential of 28.5 ± 3.8 mV. In vivo studies demonstrated that Lac-AGly/siCTGF significantly attenuated liver fibrosis, evidenced by a reduction in the collagen-positive area from 14.3% to 3.1%. Collectively, the Lac‑AGly/siCTGF nanoparticle system integrated biocompatibility, serum stability, and active hepatic targeting into a single platform, significantly improving siRNA delivery efficiency and gene‑silencing efficacy while maintaining favorable biosafety. This work provided a novel and translatable strategy for precise molecular intervention in liver fibrosis.
    Keywords:  gene transfection; glycogen; lactobionic acid; liver fibrosis; siRNA delivery
    DOI:  https://doi.org/10.1088/1361-6528/ae435b
  16. ACS Nano. 2026 Feb 07.
      Exosome (EXO) membrane proteins are attractive biomarkers for liquid biopsy, yet their heterogeneity makes it difficult to develop reliable antibody-based recognition reagents. Aptamers provide high-affinity and highly specific alternatives through the systematic evolution of ligands by exponential enrichment (SELEX), but the nanosized EXOs introduce substantial separation challenges that complicate SELEX workflows. Here, we present DeteRministic Evolution of Aptamers via a Microfluidic-integrated robotic platform (DREAMbot), an automated system engineered to execute multiround EXO-targeted aptamer selection with minimal human intervention. DREAMbot integrates a programmable pipetting robot with deterministic lateral displacement sorting and lipid-assisted magnetic isolation, enabling the automated purification and recovery of EXO-binding aptamers from cell-derived vesicles and molecular contaminants. This robotic-microfluidic workflow faithfully reproduces aptamer enrichment while substantially reducing hands-on burden compared to manual SELEX. Using cell-derived EXOs as targets, DREAMbot identified aptamers with nanomolar dissociation constants and high specificity toward GPC3-positive EXOs from both cultured cells and human serum. With its modular robotic-microfluidic architecture, DREAMbot provides a practical and accessible framework for automated aptamer discovery relevant to liquid biopsy applications.
    Keywords:  DLD sorting; aptamer SELEX; exosome; microfluidic automation; robot pipetting
    DOI:  https://doi.org/10.1021/acsnano.5c14524
  17. Research (Wash D C). 2026 ;9 1135
      The overuse and misuse of antibiotics have led to widespread resistance in bacteria, which makes infections difficult to treat. The insufficient prevention measures, limited treatment options, and delayed antibiotic developments call for immediate global actions to discover effective and safe treatments for bacterial infections. Over the past decades, more and more studies have found that bacterial extracellular vesicles (BEVs) secreted by bacteria with nanoscale size, lipid bilayer structure, pathogen-associated molecular patterns, and inherent bioactive substances are the ideal candidates for bacterial infection treatment. Meanwhile, advanced engineering approaches have further endowed these BEVs with more customizable properties to effectively fight against bacterial infections. Herein, the present review begins with an overview of the biogenesis and biocomponents of BEVs to better comprehend their bioactivities against bacterial infections. Their isolation and engineering approaches are then introduced, with an emphasis on the diverse genetic, physical, and chemical strategies to functionalize them with desirable capacities for the optimal treatment of bacterial infections. Recent advances in exploring the natural BEVs as antibacterial and antiadhesion agents, as well as the engineered BEVs as vaccine antigens, vaccine adjuvants, and delivery nanocarriers, are expounded successively. Discussions on the new trend of engineering BEVs as nanoweapons to combat bacterial infections, in terms of advantages and challenges, are provided at the end to expedite these BEV-based therapeutic modalities for bacterial infections from bench to bedside.
    DOI:  https://doi.org/10.34133/research.1135
  18. Small. 2026 Feb 07. e13436
      Peptide-based self-assembled nanostructures offer great promise for targeted drug delivery due to their intrinsic biocompatibility, biodegradability, and structural tunability. However, their limited optical properties and lack of functional sites for selective targeting restrict their use in theranostics. Here, we report a fluorophore-integrated, pH-responsive dipeptide nanocarrier engineered from phenylalanine-tryptophan (F-W) conjugated with 4-chloro-7-nitrobenzofurazan (NBD) as a fluorescent probe and vitamin B6 (VitB6) as a pH-sensitive unit. The resulting vitamin B6-modified nanoparticles (PS-Dox) exhibited charge reversal from negative to positive under mildly acidic conditions (pH 5.0), promoting doxorubicin (Dox) release, endosomal escape, and nuclear localization. PS-Dox demonstrated enhanced cytotoxicity, DNA damage, and apoptosis induction in multiple cancer cell lines, while showing negligible toxicity toward non-malignant cardiomyocytes (AC-16 and H9C2). In vivo biodistribution and pharmacokinetic studies revealed increased tumour accumulation and superior tumour growth inhibition compared with Dox. Importantly, PS-mediated encapsulation effectively mitigated Dox-associated cardiotoxicity, a major limitation of conventional chemotherapy. Overall, this study establishes a vitamin B6-mediated, charge-reversible peptide nanocarrier as a biocompatible and efficient platform for targeted anticancer drug delivery, combining tumour-specific therapeutic efficacy with improved cardiac safety.
    Keywords:  cellular imaging; pH‐responsive nanocarriers; self‐assembly; site‐specific drug delivery; vitamin B6
    DOI:  https://doi.org/10.1002/smll.202513436
  19. J Nanobiotechnology. 2026 Feb 09. 24(1): 163
      Periodontitis is a localized inflammatory condition triggered by periodontal pathogens and marked by uneven loss of alveolar bone. The clash between the persistent inflammatory environment and requirement for bone regeneration complicates the treatment of periodontitis. To address this issue, we developed a core-shell microneedles drug delivery system responsive to both high matrix metalloproteinase (MMP) expression and a local acidic microenvironment, which are the pathological characteristics of periodontal lesions. This system utilizes a dual mechanism of MMP hydrolysis and pH triggering to achieve precise spatiotemporal release of therapeutic molecules and multimodal synergistic treatment. The microneedles system utilizes a layered core-shell design: the outer shell is loaded with glycyrrhizic-acid-functionalized MIL-101, which encapsulates the core layer containing mesenchymal stem cell-derived exosomes. In the initial treatment phase, when MMP levels are elevated and pH is low, the system rapidly releases drug-loaded nanoparticles from the microneedle shell, thereby significantly inhibiting the pro-inflammatory cytokine storm and alleviating excessive oxidative stress. Subsequently, exosomes released from the microneedles core in a sustained manner contribute to rebalancing the immune microenvironment and inducing new bone formation within periodontal defects. This novel drug delivery strategy combines precise drug delivery, immune regulation, and tissue regeneration of periodontitis-associated bone defects by integrating pathological microenvironmental responsiveness, thereby overcoming the challenge of graded drug release in the complex oral environment and providing an innovative therapeutic paradigm for clinical treatment.
    Keywords:  Exosomes; Glycyrrhizic acid; Metal–organic framework; Microneedles; Periodontitis
    DOI:  https://doi.org/10.1186/s12951-026-04125-7
  20. Int J Biol Macromol. 2026 Feb 10. pii: S0141-8130(26)00779-8. [Epub ahead of print]348 150853
      Brain aging is a multifactorial process associated with oxidative stress, chronic neuroinflammation, and synaptic dysfunction, ultimately leading to cognitive decline and increased susceptibility to neurodegenerative disorders. Epigallocatechin gallate (EGCG) is a potent antioxidant and anti-inflammatory agent, but its therapeutic potential is limited by poor stability and bioavailability. In this study, a dual nano delivery system was developed by loading chitosan-EGCG nanoparticles into mesenchymal stem cell-derived exosomes (Ex-Chit-EGCG NPs) and evaluated for neuroprotective efficacy in a D-galactose-induced brain aging model. Intranasal administration of Ex-Chit-EGCG NPs significantly improved cognitive and locomotor performance compared with exosomes alone, as evidenced by enhanced outcomes in Y-maze and open field tests. Biochemical analyses revealed that Ex-Chit-EGCG NPs effectively reduced lipid peroxidation, restored glutathione levels, and reactivated the LKB1/AMPK/SIRT1 signaling pathway. Molecular investigations demonstrated upregulation of Nrf2, BDNF, and SIRT1 together with suppression of NF-κB and Iba-1 expression, indicating attenuation of oxidative and inflammatory responses. Histopathological and immunohistochemical evaluations confirmed these findings, showing preservation of cortical and brain stem architecture with marked reductions in neuronal necrosis, gliosis, BAX, GFAP, and NLRP3 expression. Collectively, the results demonstrate that Ex-Chit-EGCG NPs exert superior neuroprotective effects compared with exosomes alone, highlighting the therapeutic advantage of combining EGCG with chitosan nanocarriers and exosomal delivery. This dual nanotherapeutic strategy offers a promising and non-invasive approach for mitigating brain aging and holds potential for translation into therapies targeting age-related neurodegenerative disorders.
    Keywords:  Brain aging; Epigallocatechin gallate; Exosomes; Neuroinflammation; Oxidative stress
    DOI:  https://doi.org/10.1016/j.ijbiomac.2026.150853
  21. Acta Pharm Sin B. 2026 Feb;16(2): 1022-1045
      The modulation of tumor autophagy to enhance antitumor immunity has garnered significant attention, underscoring its critical role in cancer immunotherapy. However, advanced strategies for precise autophagy-regulating drug delivery remain a pressing need. Here, we introduce a targeted small extracellular vesicles (sEVs)-based drug delivery system capable of simultaneously loading antibodies and nucleic acid drugs while ensuring their accurate release in the tumor microenvironment (TME). We developed a dual-stimulation electroporation system that integrates nanosecond electric pulses and ultrasound to enhance sEV production, yielding IL-7 mRNA-enriched sEVs that overexpress CD64 receptors for efficient capture of anti-PD-L1 antibodies. These multifunctional autophagy-inhibiting and immunomodulatory sEVs (AI-sEVs) are designed to inhibit autophagy and modulate immune responses in non-small cell lung cancer. Upon delivery to the TME, AI-sEVs mediate the enzymatic cleavage of peptide bonds, releasing IL-7 mRNA. This process induces autophagy suppression and restores MHC-I expression, which synergizes with anti-PD-L1 immune checkpoint inhibition to enhance antitumor efficacy. In conclusion, this study proposes an innovative methodology that utilizes engineered sEVs for the co-delivery of protein antibodies and genetic materials. This approach establishes a promising strategy for advancing cancer immunotherapy by targeting the modulation of autophagy.
    Keywords:  Autophagy; Cancer immunotherapy; Drug delivery; Engineered extracellular vesicles; Interleukin-7; Non-small cell lung cancer; PD-L1; Tumor microenvironment
    DOI:  https://doi.org/10.1016/j.apsb.2025.12.013
  22. J Transl Med. 2026 Feb 09.
      
    Keywords:  Hepatic stellate cells; Human umbilical cord mesenchymal stem cell-derived exosomes; Liver fibrosis; Platelet-derived growth factor β; pPB
    DOI:  https://doi.org/10.1186/s12967-025-07658-x
  23. Front Bioeng Biotechnol. 2025 ;13 1669104
      Gene and genome editing therapies are increasingly connected with nanomaterials, which protect and transport fragile nucleic acids and CRISPR/Cas systems through biological barriers safely and accurately. This review discusses how different nanocarriers, including lipid-based, polymeric, inorganic, and vesicle-derived systems, can improve delivery efficiency, cell targeting, endosomal escape, and intracellular movement for gene and genome editing. It summarizes findings from early clinical and preclinical studies, comparing several carrier types such as ionizable lipid nanoparticles, polymeric nanoparticles, micelles, gold and silica nanostructures, and engineered extracellular vesicles. The review also explains how specific design factors, such as surface ligands, charge modification, PEGylation, and stimulus-responsive behaviors, influence biodistribution, and improve on-target efficiency while lowering immune responses and off-target effects. Ethical and regulatory concerns for in vivo editing are highlighted, along with current methods used to study nano-bio interactions. Among these carriers, ionizable lipid nanoparticles show the most advanced performance for delivering nucleic acids and CRISPR systems. However, new polymer-based and exosome-inspired carriers are progressing rapidly for repeated and targeted applications. Hybrid and responsive systems may also enable better spatial and temporal control of editing. Future research should focus on stronger in vivo potency testing, improved biocompatibility evaluation, and standardized manufacturing to ensure clinical safety and reliability.
    Keywords:  CRISPR/Cas delivery; biocompatibility; gene editing; in vivo gene therapy; lipid nanoparticles; nanocarriers; polymeric nanoparticles; targeted delivery
    DOI:  https://doi.org/10.3389/fbioe.2025.1669104
  24. PLoS Pathog. 2026 Feb;22(2): e1013908
      Plant-parasitic nematodes secrete molecules to manipulate their hosts, but little is known about their mode of delivery and packaging. Here, we describe microRNA-containing exosomes that are secreted by root-knot nematodes and systemically increase host susceptibility. By revealing a novel mode of nematode-plant communication, our findings outline a mechanism for the delivery of nematode patho-molecules, offering a new target for disrupting parasitism at the level of vesicle-mediated delivery.
    DOI:  https://doi.org/10.1371/journal.ppat.1013908
  25. Int Immunopharmacol. 2026 Feb 11. pii: S1567-5769(26)00170-0. [Epub ahead of print]174 116326
       OBJECTIVE: This study aimed to develop NGR (Asn-Gly-Arg) peptide-modified cancer-associated fibroblast (CAF)-derived exosomes for resveratrol delivery (NGR-Exos@Res) to target myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment. By inhibiting the CXCR2/NF-κB pathway, this strategy reprograms MDSC function, reverses immune suppression, restores CD8+ T-cell antitumor activity, and suppresses liver cancer (LC) progression.
    METHODS: Network pharmacology and molecular docking identified CXCR2 as a key Res target. Public scRNA-seq data analyzed MDSC-T-cell interactions in LC. Bone marrow-derived MDSCs were treated with Res in vitro; effects on CXCR2/immunosuppressive molecules were assessed via Western blot/immunofluorescence. A CAF line expressing 3×His-NGR-CD63 was generated to produce NGR-Exos loaded with Res (NGR-Exos@Res). Their toxicity, uptake, and biodistribution were evaluated. Efficacy was tested in a murine LC xenograft model, assessing MDSC function, T-cell activation, and immune evasion.
    RESULTS: Single-cell transcriptomic analysis revealed that CXCR2 was highly expressed in MDSCs within HCC tissues. Moreover, inhibitory ligand-receptor pairs such as MIF-(CD74+CXCR4) were significantly activated in the interaction network between MDSCs and T cells. In vitro experiments demonstrated that resveratrol markedly downregulated the expression of CXCR2, Arg-1, and iNOS in MDSCs, thereby suppressing their proliferation while enhancing CD8+ T-cell proliferation and IFN-γ secretion. The successfully constructed NGR-Exos@Res drug delivery system exhibited a drug encapsulation efficiency of 19.3% and improved serum stability. In vivo, treatment with NGR-Exos@Res significantly reduced tumor volume, inhibited the CXCR2/NF-κB signaling pathway, decreased the proportion of MDSCs, and enhanced CD8+ T-cell activity.
    CONCLUSION: In this study, we successfully constructed NGR peptide-modified Exos derived from CAFs for the targeted delivery of Res. This work innovatively proposes a novel immunotherapeutic strategy that targets tumor-associated MDSCs rather than directly killing tumor cells. Mechanistically, we identify and validate CXCR2 as a previously unrecognized functional target of resveratrol in MDSCs, through which resveratrol suppresses NF-κB signaling and reprograms MDSC function. Collectively, NGR-Exos@Res represents a precise and efficient delivery platform capable of reversing the immunosuppressive microenvironment in LC and provides a promising combinatorial strategy to overcome immunotherapy resistance by targeting immunosuppressive myeloid cells.
    Keywords:  CXCR2; Cancer-associated fibroblasts; Exosomes; Liver cancer; Myeloid-derived suppressor cells (MDSCs); Resveratrol; Tumor microenvironment
    DOI:  https://doi.org/10.1016/j.intimp.2026.116326
  26. J Nanobiotechnology. 2026 Feb 13.
      CRISPR-Cas9, an innovative genome-editing technique, holds immense promise in therapeutic applications; nevertheless, the lack of effective delivery methods for in vivo gene editing limits its utility in osteoarthritis (OA) treatment. Recently, exosomes, naturally derived nanosized vesicles secreted by cells, have attracted significant attention as potential vehicles for therapeutic cargo delivery. This study proposes a bioinspired engineered exosome-mediated CRISPR/Cas9 delivery platform for targeted editing of the Asporin (ASPN) gene as a potential precision therapy for OA. Specifically, chondrocyte affinity peptide (Cap)-modified MSC-derived exosomes were employed as natural, biocompatible carriers to deliver CRISPR/Cas9 components specifically to OA-affected chondrocytes, thereby achieving precise and efficient ASPN knockout. Flow cytometry analysis confirmed a modification efficiency of 79.1% for Cap, while the encapsulation efficiency of the ASPN-Cas9 plasmid into exosomes reached 9.5% ± 0.6%. Both in vivo and in vitro investigations revealed that this delivery approach markedly improved cellular uptake and gene-editing efficacy, achieving a substantial reduction of ASPN expression by 61.7%. This, in turn, alleviated ferroptosis, improved mitochondrial function, reduced chondrocyte senescence, inhibited inflammation, and enhanced the cartilage microenvironment. Altogether, these findings strongly suggest the promising therapeutic efficacy of this method in OA models, emphasizing its potential as a precise gene-targeting therapeutic intervention for OA.
    Keywords:  ASPN; CRISPR/Cas9; Exosomes; Ferroptosis; Osteoarthritis
    DOI:  https://doi.org/10.1186/s12951-026-04158-y
  27. Carbohydr Polym. 2026 Apr 15. pii: S0144-8617(26)00054-8. [Epub ahead of print]378 124938
      The plant-derived photoactivated fungicide α-Terthienyl (α-T) exerts antimicrobial effects through light-induced reactive oxygen species generation. However, its agricultural application has been constrained by poor targeting capability and low photostability. To address these challenges, we developed a dual-responsive nanoparticle delivery system (α-T NPs) based on a pectin-chitosan polymer network that specifically recognizes the acidic and pectinase-rich microenvironment created by Botrytis cinerea hyphae secretions. Controlled release studies demonstrated that both acidic conditions (pH 5.0) and pectinase exposure substantially promoted α-T release, achieving cumulative release rates of 71.73% and 74.49% respectively over 60 h. The nanoparticle system showed no adverse effects on healthy tomato leaf growth while forming a protective barrier that effectively suppressed fungal infection. Targeted delivery significantly enhanced fungicidal efficacy, with α-T NPs exhibiting an EC₅₀ of 0.419 mg/L compared to 1.943 mg/L for α-T (technical material, TC). Confocal microscopy and quantitative analysis confirmed the enhanced targeting mechanism, revealing substantially stronger fluorescence intensity and higher α-T accumulation specifically on treated fungal hyphae. Additionally, α-T NPs significantly improved photostability, extending the half-life by approximately 1.93-fold under continuous illumination compared to α-T (TC). This work establishes an innovative "pathogen-activated" delivery platform with promising applications in sustainable crop protection.
    Keywords:  Botrytis cinerea; Chitosan; Pectin; Photostability; Stimuli-responsive release; Α-Terthienyl
    DOI:  https://doi.org/10.1016/j.carbpol.2026.124938
  28. Transl Cancer Res. 2026 Jan 31. 15(1): 59
       Background: Rho GTPase-activating protein 11A (ARHGAP11A) and family with sequence similarity 83, member A (FAM83A) play important roles in tumor development. However, the mutual regulatory relationship and mechanism of action between ARHGAP11A and FAM83A in lung adenocarcinoma (LUAD) and pancreatic adenocarcinoma (PAAD) are still unclear. This study investigated the role of the ARHGAP11A-FAM83A regulatory network in LUAD/PAAD progression via bioinformatics and experimental analyses.
    Methods: In this study, 33 tumor-related sequencing datasets were downloaded from The Cancer Genome Atlas (TCGA) database, and relevant tumor tissues were collected to explore which tumors showed the highest correlation between ARHGAP11A and FAM83A. A Gene Set Enrichment Analysis (GSEA) was conducted to identify common enrichment pathways and the significantly different proteins of ARHGAP11A and FAM83A. The protein and gene expression of ARHGAP11A and FAM83A were also knocked down to explore the regulatory relationship and mechanism of ARHGAP11A and FAM83A in tumors. Univariate and multivariate Cox regression and receiver operating characteristic (ROC) curve analyses were conducted to establish and evaluate a prognostic model based on ARHGAP11A and FAM83A (risk model), and to explore the correlation of the model with patient clinical and pathological parameters. Finally, lactate and glucose content, Cell Counting Kit-8 (CCK-8), tablet cloning, flow cytometry cycles, apoptosis, and membrane potential experiments were performed to explore the roles of ARHGAP11A and FAM83A in tumor progression.
    Results: After a series of studies, we found a strong correlation between ARHGAP11A and FAM83A in LUAD and PAAD across 33 tumor types. In the collected tumor and adjacent cancer groups, the correlation between ARHGAP11A and FAM83A was significant and highly distributed in the LUAD and PAAD groups. Meanwhile, ARHGAP11A and FAM83A were significantly enriched in the MYC, MTORC1, and glycolysis-related pathways. A series of related and intersection analyses revealed that ARHGAP11A and FAM83A were highly correlated with lactate dehydrogenase A (LDHA). Western blot and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) experiments showed that the expression of ARHGAP11A had a significant effect on FAM83A and LDHA. Additionally, FAM83A also affected LDHA expression. The risk model played an important role in patient diagnosis and prognosis. Further, this risk model served as a superior independent prognostic factor compared with other clinical and pathological parameters. Finally, the knock down of ARHGAP11A and FAM83A significantly affected the glycolysis, proliferation, apoptosis resistance, cell-cycle progression, migration, invasion, and mitochondrial membrane potential of LUAD and PAAD cells.
    Conclusions: This study showed that ARHGAP11A affects the occurrence and development of LUAD and PAAD by regulating the expression of FAM83A. This study also provides a new perspective for later tumor treatment.
    Keywords:  Lung adenocarcinoma (LUAD); Rho GTPase-activating protein 11A (ARHGAP11A); family with sequence similarity 83, member A (FAM83A); glycolysis and prognostic diagnosis; pancreatic adenocarcinoma (PAAD)
    DOI:  https://doi.org/10.21037/tcr-2025-1961
  29. Mediators Inflamm. 2026 ;2026 7251718
       Background and Objective: Diabetic retinopathy (DR) is a leading cause of vision loss in patients with diabetes mellitus (DM), and its pathogenesis is closely associated with aberrant microglial activation. Although bone marrow mesenchymal stem cell-derived exosomes (BMSC-Exo) and the miRNAs that they carry show therapeutic potential for DR, the specific roles and molecular mechanisms through which let-7b-5p regulates microglial activation after it is delivered by BMSC-Exo remain unclear. This study aimed to elucidate the function and underlying mechanism of BMSC-Exo let-7b-5p in DR.
    Methods: A DR mouse model was established by intraperitoneal injection of streptozotocin (STZ), and BV-2 microglia were stimulated with high glucose (HG) to induce activation in vitro. The morphological characteristics of the BMSC-Exo were identified using transmission electron microscopy (TEM). Protein and gene expression levels, as well as microglial activation, were assessed by Western blot, RT-qPCR, and immunofluorescence, respectively. Retinal tissue damage and apoptosis were evaluated using HE staining and TUNEL assays.
    Results: BMSC-Exo treatment significantly suppressed the expression of activation markers (Iba1 and TSPO) and inflammatory cytokines (TNF-α, IL-1β, and IL-6) in HG-induced BV-2 cells and DR mouse retinas while alleviating retinal tissue damage and apoptosis. Bioinformatics analysis revealed the downregulation of let-7b-5p in DR. Functional experiments demonstrated that let-7b-5p overexpression enhanced the inhibitory effects of BMSC-Exo on microglial activation, inflammation, and retinal damage, whereas let-7b-5p knockdown attenuated these therapeutic benefits. Mechanistically, BMSC-Exo let-7b-5p inhibited excessive microglial activation and inflammatory responses by targeting the TLR4/ATF4 signaling pathway.
    Conclusion: BMSC-Exo deliver let-7b-5p to suppress the TLR4/ATF4 pathway, thereby mitigating microglial activation and inflammation and ultimately delaying DR progression. These findings support the potential of this novel therapeutic strategy for targeted DR treatment.
    Keywords:  TLR4/ATF4 pathway; bone marrow mesenchymal stem cells; diabetic retinopathy; exosomes; let-7b-5p; microglial cell activation
    DOI:  https://doi.org/10.1155/mi/7251718
  30. Mol Pharm. 2026 Feb 10.
      Pancreatic cancer presents significant imaging challenges due to its poor vascularization, while the hypoxic tumor microenvironment further contributes to chemoresistance. To address these limitations, we engineered exosome-ultrasmall iron oxide (Exo-USIO), a targeted exosomal nanoprobe encapsulating USIO nanoparticles (USIO NPs), designed to enable precise tumor imaging and enhance chemotherapy efficacy in pancreatic cancer. Exosomes derived from Panc-02 pancreatic cancer cells were isolated and loaded with USIO NPs via electroporation to synthesize Exo-USIO. The nanoprobe's targeting specificity, MRI contrast enhancement, and catalase-like activity (converting H2O2 to O2) were systematically evaluated. In vitro assays assessed cellular uptake, hypoxia modulation, and chemosensitivity, while in vivo studies validated tumor-targeted MRI imaging, hypoxia alleviation, and synergistic therapeutic effects with gemcitabine (GEM). Exo-USIO demonstrated a 2.3-fold increase in T1-weighted MRI signal intensity compared to free USIO NPs (P < 0.01), alongside efficient enzymatic conversion of H2O2 to O2, significantly reducing HIF-1α expression (P < 0.05). Combined with GEM, Exo-USIO reduced tumor cell viability to 39.8% in vitro and suppressed tumor growth by 62% in vivo (P < 0.001). Biosafety evaluations revealed negligible systemic toxicity or metastatic risk. By leveraging exosome-mediated targeted delivery and the dual enzyme-mimetic activity of USIO NPs, Exo-USIO achieves dual functionality: enhanced MRI-guided tumor localization and catalytic alleviation of hypoxia to reverse chemoresistance. This strategy overcomes key limitations of the pancreatic tumor microenvironment, offering a translatable platform for precision theranostics.
    Keywords:  MRI; Nanozyme; Pancreatic cancer; Ultrasmall iron oxide nanoparticles
    DOI:  https://doi.org/10.1021/acs.molpharmaceut.5c01556
  31. Am J Transl Res. 2026 ;18(1): 236-247
       OBJECTIVES: Patients with type 2 diabetes mellitus (T2DM) exhibit accelerated atherosclerosis progression and an increased risk of cardiovascular disease (CVD). Early CVD diagnosis and timely intervention are critical to mitigate complications and mortality in this population.
    METHODS: Serum exosomes were isolated from 12 T2DM patients with or without carotid atherosclerosis (CAS). miRNA profiling was performed using microarray analysis. A total of 187 T2DM patients were divided into the test and validation cohorts. Plasma-derived exosomal miRNAs were quantified using quantitative PCR (qPCR), and their diagnostic potential was assessed using receiver operating characteristic curve analysis and area under the curve (AUC) calculations.
    RESULTS: Microarray analysis identified 23 differentially expressed miRNAs (DEMIs), including 19 upregulated and 4 downregulated miRNAs. Four of these (hsa-miR-433-3p, hsa-let-7b, hsa-miR-30-5p, and hsa-miR-122-5p) were significantly elevated in patients with CAS and showed positive correlation with carotid intima-media thickness. The results also showed that these miRNAs demonstrated diagnostic efficacy for CAS detection in patients with T2DM, and were stratified by disease severity.
    CONCLUSIONS: The identified miRNA panel represents a promising diagnostic biomarker for CAS in patients with T2DM, providing a foundation for the development of targeted therapies to address diabetic cardiovascular complications.
    Keywords:  Exosomes; atherosclerosis; carotid intima-media thickness; diabetes; miRNA
    DOI:  https://doi.org/10.62347/UWCR7720
  32. Mol Cell Probes. 2026 Feb 06. pii: S0890-8508(26)00004-6. [Epub ahead of print]86 102064
      Stem cell-derived and plant-derived exosomes are emerging as promising therapeutic agents in cutaneous repair, regeneration, and rejuvenation. They facilitate wound healing and skin revitalization through multifaceted mechanisms, including immunomodulation, promotion of cellular differentiation, and stimulation of angiogenesis. Additionally, their ability to modulate collagen production and remodeling underscores their potential in addressing skin aging and improving cosmetic outcomes. Consequently, exosome-based therapies show promise for a range of conditions, from challenging wounds and skin aging to pigmentary disorders, hair loss, certain immune-mediated dermatoses. To ensure a comprehensive and unbiased synthesis of the current evidence, this systematic review was conducted following a structured methodology, encompassing a search across multiple major databases over a defined 20-year period. This review systematically outlines the roles and applications of commonly employed plant exosomes and stem cell exosomes in recent years' advancements in skin repair and cosmetic dermatology. By synthesizing the current understanding of their mechanisms and clinical potential, this review aims to highlight viable therapeutic strategies that bridge the gap between medical dermatology and aesthetic medicine.
    Keywords:  Cutaneous medical aesthetics; Plant exosomes; Skin regeneration; Stem cell exosomes
    DOI:  https://doi.org/10.1016/j.mcp.2026.102064
  33. Tissue Eng Regen Med. 2026 Feb 12.
       BACKGROUND: Sensorineural hearing loss caused by ototoxic agents remains irreversible due to the limited regenerative capacity of cochlear hair cells. Exosome-based therapies derived from mesenchymal stem cells (MSCs) offer a promising, cell-free alternative to protect auditory structures by modulating oxidative stress and inflammation. In this study, we evaluated the therapeutic potential of exosomes isolated from nanoparticle (NP) labeled, N-acetylcysteine primed tonsil-derived mesenchymal stem cells (T-MSCs), hereafter referred to as SPISOME-NAC, in kanamycin-induced ototoxicity models.
    METHODS: T-MSCs were labeled with positively charged PLGA-PEI clustered SPIONs, with or without NAC pretreatment. Antioxidant enzyme activity (SOD, CAT, GSH), ROS levels, and PRDX1 expression were assessed in vitro. Exosomes were isolated and analyzed via nanoparticle tracking analysis. Their therapeutic efficacy was evaluated in both ex vivo cochlear explants and mouse model of kanamycin-induced ototoxicity. Hair cell survival was quantified via Myosin VIIa immunostaining, and auditory function was assessed using auditory brainstem responses (ABR). Pro-inflammatory cytokines (TNF-α, IL-1, IL-6) were measured via qRT-PCR.
    RESULTS: NAC pretreatment significantly enhanced cell viability, increased GSH activity, and reduced intracellular ROS and PRDX1 levels in NP-labeled T-MSCs. Exosomes derived from NAC-pretreated cells (SPISOME-NAC) conferred superior protection to cochlear hair cells, particularly in the basal turn, and significantly improved hearing thresholds in vivo. Furthermore, SPISOME-NAC treatment downregulated inflammatory cytokines in cochlear tissue.
    CONCLUSION: SPISOME-NAC exhibit enhanced antioxidant and anti-inflammatory properties, providing functional protection in an ototoxicity-induced hearing loss model. By preventing ROS-mediated mitochondrial damage and apoptosis in cochlear hair cells, NAC interrupts a key pathogenic mechanism in ototoxicity, preserving auditory structure and function. These findings support NAC-primed exosomes as a novel therapeutic strategy for sensorineural hearing loss.
    Keywords:  Antioxidant; Hearing loss; Mesenchymal stem cell
    DOI:  https://doi.org/10.1007/s13770-025-00784-z
  34. Endocr J. 2026 Feb 06.
      Osteoporosis (OP) is a metabolic bone disease characterized by impaired bone formation and excessive resorption. Ferroptosis has been implicated in osteoblast dysfunction. Adipose-derived stem cell exosomes (ADSC-exos) have emerged as promising regenerative therapies. This study investigated whether ADSC-exos alleviate ferroptosis and promote osteogenic differentiation by modulating the miR-215-5p/USP1/PTEN/AKT/GSK3β/NRF2 pathway. Human ADSC-exos were evaluated using transmission electron microscopy, nanoparticle tracking analysis, and western blot. Ferroptosis was induced in MG63 cells using ferric ammonium citrate (FAC). Cell viability, lipid peroxidation, and osteogenic differentiation were evaluated using the CCK-8 assay, C11-BODIPY staining, malondialdehyde quantification, ALP staining, and Alizarin Red S staining. The effects of ADSC-exos on PTEN ubiquitination and AKT/GSK3β/NRF2 pathway activation were assessed using western blot, RT-qPCR, and immunoprecipitation. ADSC-exos significantly improved osteoblast viability, reduced lipid peroxidation, and enhanced osteogenic differentiation in FAC-treated MG63 cells. Dual-luciferase reporter assay identified miR-215-5p as a key exosomal cargo that targets USP1. Mechanistically, ADSC-exos downregulated USP1, leading to PTEN ubiquitination and degradation, thereby activating the AKT/GSK3β/NRF2 signaling pathway. USP1 overexpression reversed the protective effects of ADSC-exos, confirming that miR-215-5p-mediated USP1 inhibition plays a crucial role in regulating ferroptosis and osteogenic differentiation. In conclusion, ADSC-exos diminish ferroptosis and enhance osteogenic differentiation by delivering miR-215-5p, which inhibits USP1, promotes PTEN ubiquitination, and activates the AKT/GSK3β/NRF2 pathway. These findings provide new insights into the mechanisms by which ADSC-exos promote bone repair and highlight their potential as an innovative treatment for OP.
    Keywords:  Exosomes; Ferroptosis; MiR-215-5p; Osteoporosis; Ubiquitin-specific protease 1 (USP1)
    DOI:  https://doi.org/10.1507/endocrj.EJ25-0336
  35. J Nanobiotechnology. 2026 Feb 11. 24(1): 159
      Exosomes are nanoscale extracellular vesicles that transfer proteins, nucleic acids, and lipids, reflecting the state of their parent cells. A persistent scientific challenge is that tumor-derived exosomes (TDEs) facilitate immune evasion, remodel the tumor microenvironment, and create premetastatic niches, intensifying tumor aggressiveness and undermining therapeutic efficacy, ultimately narrowing treatment options to palliative strategies in advanced settings. Yet their dual roles as suppressive agents and potential therapeutic tools remain poorly integrated within current cancer immunotherapy frameworks. This review examines the molecular mechanisms underlying TDE-mediated immune suppression and therapeutic resistance, while also highlighting engineering strategies to exploit or counteract exosome biology. Exosomes derived from chimeric antigen receptor (CAR) T cells preserve antigen specificity and cytotoxic components without the risks of uncontrolled proliferation or cytokine release, offering a safer class of cell free immunotherapies. Advances in genetic engineering, hybrid vesicle design, and nanotechnology have extended exosome applications to the delivery of CRISPR/Cas systems, chemotherapeutic agents, immunoregulatory RNAs, and vaccines, with liposome or nanoparticle integration enhancing targeting and efficacy. Remaining obstacles include the lack of standardized protocols, scalability issues in production, and unresolved regulatory frameworks. Drawing on The Art of War, exosomes can be envisioned as avatars of strategy, discreet messengers capable of undermining host defenses while simultaneously carrying the potential to redirect immunity against the tumor. By embodying both deception and counterattack, they illustrate the capacity to penetrate hidden barriers and redefine the therapeutic battlefield, opening new horizons for precision cancer immunotherapy.
    Keywords:  CAR-T exosomes; CRISPR/Cas9 delivery; Cancer resistance; Cell-free therapy; Chimeric antigen receptor (CAR) t cells; Drug delivery; Exosome engineering; Exosomes; Extracellular vesicles (EVs); Immune suppression; Immunotherapy; Nanotechnology; Pre-metastatic niche; Tumor microenvironment (TME); Tumor-derived exosomes (TDEs)
    DOI:  https://doi.org/10.1186/s12951-026-04089-8
  36. Adv Sci (Weinh). 2026 Feb 12. e21802
      Autoimmune diseases (ADs) are chronic disorders caused by a breakdown in immune self-tolerance, triggering aberrant immune attacks against one's own tissues. These responses cause persistent inflammation and multiorgan damage. As the global prevalence of ADs continues to increase, they impose a growing public health burden, but current treatments do not meet clinical needs. Extracellular vesicles (EVs) are lipid bilayer membrane-enclosed nanoparticles secreted by live cells that can carry diverse bioactive molecules and play essential roles in intercellular communication. Recently, EVs have attracted considerable attention as promising therapeutic candidates for ADs owing to their high biocompatibility, low immunogenicity, and ability to traverse biological barriers. This review systematically summarizes the current applications and development trends of both plant and mammalian sources and explores the functions of natural or engineered EVs in modulating the pathological processes underlying ADs. We also discuss the emerging potential of EVs as diagnostic biomarkers and targeted drug delivery systems for autoimmune conditions. Although clinical translation of EV-based therapies faces challenges, deepening our understanding of the pathogenic roles of EVs in autoimmunity coupled with ongoing advances in bioengineering technologies holds promise for delivering novel theoretical insights and practical strategies for diagnosing and treating these refractory diseases.
    Keywords:  autoimmune diseases; extracellular vesicles; isolation and engineering; mechanism of action; therapeutic applications
    DOI:  https://doi.org/10.1002/advs.202521802
  37. J Control Release. 2026 Feb 07. pii: S0168-3659(26)00082-9. [Epub ahead of print]392 114681
      Current therapies for autoimmune diseases largely rely on broad-spectrum immunosuppressants and biologics, which indiscriminately deplete T or B cells. These approaches are largely constrained by systemic immunosuppression and off-target toxicities. Achieving durable, antigen-specific immune tolerance while preserving protective immunity against pathogens remains a long-standing goal in clinical practice. Here, we present a modular red blood cell (RBC)-based platform that induces antigen-specific tolerance through strain-promoted azide-alkyne cycloaddition (SPAAC)-mediated surface conjugation of disease-relevant peptides. We demonstrated that RBCs engineered by such approach retain their biophysical integrity and biocompatibility across a broad range of conjugation concentrations in vitro. Critically, when conjugated with single or multiple autoantigenic epitopes, these engineered RBCs elicited robust antigen-specific tolerance and drove durable disease remission in two well-established preclinical models, experimental autoimmune encephalomyelitis (EAE) and collagen-induced arthritis (CIA). Further mechanistic investigations revealed that the engineered RBCs reprogram antigen-presenting cells (APCs) toward a tolerogenic phenotype. This reprogramming, in turn, induces anergy in autoreactive T cells and suppresses the activation of autoreactive B cells. Collectively, this work establishes a versatile and clinically translatable platform, offering a path toward personalized, antigen-specific therapy for autoimmune diseases.
    Keywords:  Antigen-specific tolerance; Click chemistry; Collagen-induced arthritis; Experimental autoimmune encephalomyelitis; Red blood cells
    DOI:  https://doi.org/10.1016/j.jconrel.2026.114681
  38. Crit Rev Microbiol. 2026 Feb 09. 1-15
      The human microbiome, comprising trillions of microorganisms across multiple body sites, is increasingly recognized as a key contributor to host immunity, metabolism, and neurobiology, influencing development and disease susceptibility throughout life. Rather than acting in isolation, microbial communities operate within a complex host-environment system shaped by genetics, diet, lifestyle, and medical exposures. Conceptually, the microbiome can be understood as part of a host-microbe meta-organism and, from a translational perspective, as a dynamic and potentially modifiable organ system. While short-term perturbations such as antibiotics may transiently disrupt microbial ecosystems, persistent maladaptive configurations, commonly termed dysbiosis, are associated with metabolic disease, chronic inflammation, neurodevelopmental disorders, and cancer, although causality remains context dependent. This review synthesizes the functional roles of beneficial microbes and their metabolites, the mechanistic and clinical implications of dysbiosis, and immune pathways shaped by microbial signals. We further discuss emerging therapeutic strategies, including dietary modulation, probiotics, engineered microbial consortia, postbiotics, and fecal microbiota transplantation, enabled by multi-omics technologies, organoid models, and computational frameworks. Key challenges include defining context-specific microbial health, ensuring durable engraftment, and addressing regulatory and ethical considerations. Framing the microbiome as a dynamic component of host physiology provides a foundation for microbiome-guided precision and preventive medicine.
    Keywords:  Human microbiota; dysbiosis; host immunity; human health; microbiota-based precision medicine
    DOI:  https://doi.org/10.1080/1040841X.2026.2629269
  39. Comb Chem High Throughput Screen. 2026 Feb 04.
      <p> Introduction: Asthma is characterized by chronic airway inflammation and Th1/Th2 immune imbalance. Wuhu decoction (WHD), a classic formulation in Traditional Chinese Medicine, has demonstrated significant clinical efficacy in managing asthmatic exacerbations. However, the precise molecular mechanisms by which WHD ameliorates airway inflammation in asthma remain inadequately characterized. This work was undertaken to assess the protective actions of WHD in alleviating airway inflammation in asthmatic rats and to explore potential mechanisms. </p> <p> Methods: A total of Eighty female SD rats were used. Twenty rats served as unsensitized controls, and sixty were sensitized with Al(OH)3 and ovalbumin (OVA) to induce asthma. After successful modeling, they were randomly classified into control, model, dexamethasone, and low, medium, and high-dose WHD groups and received corresponding drug intervention for two weeks. Airway reactivity was recorded using plethysmography; lung tissue histological changes were assessed by PAS, H&E, and Masson staining; Gamma-interferon (IFN-γ), interleukin-4 (IL-4), and immunoglobulin E (IgE) serum levels were determined by ELISA; qRT-PCR was used to detect miR-155 in rat lung tissues; Western blot determined GATA3 and T-bet proteins levels in lung tissues of rats; Pearson correlation evaluated correlation between miRNA-155 levels in lung tissues of asthmatic rats and T-bet, GATA3. </p> <p> Results: The results of airway reactivity indicated successful replication of the asthma rat model. The airway reactivity index in model rats increased significantly by 115.3%, accompanied by elevated inflammatory cells around the trachea and bronchi, excessive proliferation of epithelial cells, and widespread deposition of airway collagen when compared to controls. Serum IL-4 and IgE levels were elevated by 172.7% and 69.2%, while IFN-γ expression was reduced by 38.8%, and miR-155 expression in lung tissue was increased by 187.8% in model rats compared to controls. T-bet expression decreased, while GATA3 expression increased significantly in lung tissues from asthma rats compared to controls. Compared to model rats, both WHD and dexamethasone treatment significantly reduced the airway hyperresponsiveness in rats, alleviated lung tissue damage, reduced epithelial cell proliferation and airway collagen deposition, decreased serum IgE and IL-4 levels, elevated IFN-γ levels, and simultaneously reduced miR-155 expression, GATA3 protein level, and increased T-bet protein level in lung tissues. The miRNA-155 in asthmatic rat lung tissues was negatively correlated with T-bet (r = - 0.1441; P < 0.001), and positively correlated with GATA3 (r = 0.04578; P < 0.0001). </p> <p> Discussion: This study demonstrates that WHD exerts protective effects against allergic airway inflammation in asthmatic rats by modulating immune responses. WHD treatment significantly attenuated airway hyperresponsiveness, reduced epithelial cell proliferation, mucus secretion, and collagen deposition. The inverse correlation between miR-155 and T-bet, along with the positive association with GATA3, suggests that WHD may alleviate asthma through miR-155/T-bet/GATA3 axis. These findings highlight WHD as a promising traditional therapy with potential molecular targets for future asthma interventions. </p> <p> Conclusion: WHD effectively alleviated airway inflammation in asthmatic rats, and the protective effects were associated with inhibiting miR-155 levels in lung tissue, regulating T-bet/GATA3 imbalance, and reducing the secretion of inflammatory factors IL-4 and IgE. </p>.
    Keywords:  T-bet/GATA3; Wuhu decoction; asthma; dexamethasone; lung tissues.; miR-155
    DOI:  https://doi.org/10.2174/0113862073402170251012174133
  40. Mar Biotechnol (NY). 2026 Feb 09. 28(1): 29
      The high concentration of ammonia from deteriorated aquaculture environments and intensive culture system increases the susceptibility to white spot syndrome virus (WSSV) and causes high mortality in Pacific white shrimp Litopenaeus vannamei. However, its molecular mechanism remains to be elucidated. In the present study, small RNA sequencing was performed for understanding the molecular mechanism of acute ammonia toxicity increasing susceptibility to WSSV in Pacific white shrimp with the individuals under normal conditions (LC group), ammonia stress (LA group), WSSV infection (LV group), and WSSV infection with ammonia stress (LAV group). Compared with other groups, more significantly upregulated differentially expressed miRNAs (DEMs) were identified in the LAV group, which targeted to the immune-, energy metabolism-, and ROS scavenging-related genes. The KEGG enrichment analysis showed that the target genes of the DEMs in LA and LAV groups (both with ammonia stress) were specially involved in viral carcinogenesis, and those in LAV group were also specially involved in hippo signaling pathway and chemokine signaling pathway. The copper zinc superoxide dismutase (Cu/Zn-SOD) was predicted as the target gene of the specific DEMs of novel_59 and novel_71 in the LAV group. The mRNA expression and enzyme activity of Cu/Zn-SOD was significantly lower in the LAV group than other groups, but the ROS production rate was the highest in the LAV. This study provides new insights for understanding the molecular mechanism of high WSSV-infection under ammonia toxicity in shrimps from the post-transcriptional perspective.
    Keywords:   Litopenaeus vannamei ; Ammonia stress; ROS; SOD; Small RNA; WSSV
    DOI:  https://doi.org/10.1007/s10126-026-10571-z
  41. Annu Rev Biomed Eng. 2026 Feb 10.
      Cells exist along a spectrum from viable to dead. Yet most cell engineering has focused primarily on the live state. This review explores how controlled manipulation of cell death or arrest can be used to build effective, safer, and more predictable therapies. By engineering apoptosis, irreversible growth arrest, or synthetic gene circuits, cells can be programmed for functional outputs without relying on full viability. These approaches reduce heterogeneity, improve stability, and extend the therapeutic window. We introduce a framework for understanding engineered living, dying, and dead cell therapies on the basis of their activity, functions, and applications. Across this spectrum, engineered cells show promise for applications in immune modulation, drug delivery, and tissue regeneration. We also examine key methods that enable these designs, including genetic, physical, and materials-based tools. This perspective offers a path toward programmable and consistent cell-based therapies across diverse biomedical domains.
    DOI:  https://doi.org/10.1146/annurev-bioeng-110824-021221
  42. Phytomedicine. 2026 Feb 07. pii: S0944-7113(26)00175-3. [Epub ahead of print]153 157937
       BACKGROUND: Knee osteoarthritis (KOA) represents a chronic degenerative disorder associated with functional disability. Synovitis constitutes a major driver of KOA progression and clinical deterioration. Cyasterone (CYA) exerts therapeutic effects on KOA, yet its underlying mechanism remains undefined.
    PURPOSE: This study integrated non-targeted metabolomics with molecular biology approaches to investigate the therapeutic potential of CYA in KOA rats.
    METHODS: A KOA model was established by ACLT. After CYA intervention at graded concentrations, synovial tissue was subjected to pathological assessment and inflammatory evaluation. Non-targeted metabolomics was performed to characterize metabolic alterations. Fibroblast-like synovial cells (FLS) were isolated, and after group-specific treatment, analyses included EdU staining, Hoechst 33,342/PI double staining, flow cytometry, immunofluorescence, transmission electron microscopy (TEM), mRFP-GFP-LC3 puncta assay, Western blotting, and q-PCR. Molecular docking, molecular dynamics simulation (MDS), and surface plasmon resonance (SPR) techniques were explored the binding potential between CYA and the AMPK.
    RESULTS: Histopathological analysis demonstrated that CYA significantly alleviated synovitis progression in KOA. Metabolomics revealed extensive metabolic dysregulation in KOA, with CYA intervention restoring lipid metabolic balance. Molecular assays showed that CYA attenuated inflammatory cytokine production, suppressed FLS proliferation, and enhanced FLS apoptosis during KOA progression. Mechanistically, CYA regulated lipid metabolism in FLS through AMP-activated protein kinase (AMPK) activation, characterized by increased p-ACC and CPT1 expression, decreased FASN, SREBP-1, and SCD-1 expression, elevated GSH levels, reduced MDA accumulation, and diminished neutral lipid droplets. CYA also promoted AMPK-dependent autophagy, evidenced by upregulation of p-ULK1, LC3B, and Beclin1, concomitant downregulation of P62, enhanced autophagosome formation, and increased autophagic flux. Subsequent validation confirmed that modulation of lipid metabolism and autophagy via the AMPK pathway accounted for the protective effects of CYA against KOA synovitis. Molecular docking, MDS, and SPR results indicate that CYA exhibits high affinity for the AMPK protein.
    CONCLUSION: CYA activates AMPK signaling, restores lipid metabolic homeostasis, and enhances autophagy, thereby mitigating KOA synovitis.
    Keywords:  AMPK; Autophagy; Cyasterone; Knee osteoarthritis; Lipid metabolism; Synovitis
    DOI:  https://doi.org/10.1016/j.phymed.2026.157937
  43. Clin Exp Immunol. 2026 Feb 13. pii: uxag009. [Epub ahead of print]
      Exosomes, the nanoscale extracellular vesicles released by most cell types, are increasingly recognised as potent regulators of immune communication. This review provides a mechanistic and integrative perspective on the immunological functions of exosomes, highlighting their roles in both immune stimulation and suppression across physiological and pathological contexts. We begin by dissecting the molecular architecture of exosomes-focusing on immunologically active components such as ESCRT proteins, tetraspanins, RabGTPases, and lipid mediators-and explore how these elements contribute to exosome biogenesis and immune function. The review further examines exosomal cargo enriched in pattern recognition receptor ligands, including TLRs, DAMPs, PAMPs, and miRNAs, and discusses how these molecules orchestrate innate immune responses through endosomal and cytosolic signaling cascades. Special emphasis is given to MHC-mediated antigen presentation via exosomes, distinguishing classical and non-canonical pathways and their interplay with mechanisms. We present a dichotomous view of exosomes as both immunostimulatory and immunosuppressive agents, detailing their roles in T cell cross-priming, dendritic cell maturation, tumor progression, and metastasis. Moreover, we review pathogen-driven hijacking of exosomal pathways and their implications for immune evasion. Finally, we discuss the therapeutic promise of exosomes in cancer immunotherapy and vaccine design, advocating for their strategic integration into next-generation immunomodulatory approaches.
    Keywords:  Antigen Presentation; Exosomes; Extracellular Vesicle Signaling; Immune Modulation; Pattern Recognition Receptors (PRRs)
    DOI:  https://doi.org/10.1093/cei/uxag009
  44. J Mater Chem B. 2026 Feb 10.
      An [AzA][Nic] cocrystal was engineered through supramolecular synthon design between azelaic acid ([AzA]) and nicotinamide ([Nic]) to overcome intrinsic [AzA] bioavailability limitations. Single-crystal X-ray analysis and DFT calculations revealed that the N1⋯O4-H4 hydrogen bond and electrostatic complementarity drive molecular reorganization into a distinctive cocrystal architecture. This supramolecular restructuring induces critical conformational shifts of [Nic] and [AzA], leading to a 9.6-fold enhancement in the aqueous solubility of [AzA] (from 2.4 to 23 mg mL-1) and a reduced HOMO-LUMO gap to 8.159 eV (vs. 9.926 eV for [AzA]) with stronger electron-donating/accepting capabilities and multiple active sites, which facilitates the bioactivity and bioavailability of [AzA]. Computational docking demonstrated the cocrystal's superior PPARγ binding (ΔGbinding = -153.5 kJ mol-1) and stable complex formation (evidenced by reduced Rg and SASA), mechanistically explaining its ability to suppress pro-inflammatory cytokines (TNF-α/IL-8/PGE-2) and reduce melanin levels in vitro. Clinical validation of 3 wt% essence confirmed significant human skin brightening (increase in L/ITA°, p < 0.01) and depigmentation (decrease in M, p < 0.05). This work establishes cocrystallization as a transformative supramolecular strategy for optimizing dermatological activities by utilizing synergistic structure-bioactivity relationships.
    DOI:  https://doi.org/10.1039/d5tb02498f
  45. Am J Chin Med. 2026 ;54(1): 201-228
      The global incidence and prevalence of autoimmune diseases are increasing, and there is thus a need to develop novel, effective, and affordable therapeutic agents for autoimmune diseases. Triptolide (TP), a bioactive diterpenoid epoxide isolated from Tripterygium wilfordii Hook F, exhibits potent immunosuppressive and anti-inflammatory activities, and can be a potential therapeutic for multiple autoimmune diseases. The therapeutic effects of TP can be attributed to multiple mechanisms, including the inhibition of T cell and B cell activation, the restoration of T helper 17 cell/regulatory T cell balance, the suppression of pro-inflammatory cytokines, and the modulation of critical signaling pathways like the NF-κB, JAK/STAT, and PI3K/Akt pathways. TP alleviates pathological conditions by regulating oxidative stress responses and influencing gut microbiota composition. However, the clinical application of TP is limited due to severe dose-dependent and time-dependent toxic effects on the liver, kidneys, reproductive system, and other organs. Recent studies have highlighted several strategies, such as chemical structure modification, nanocarrier-based delivery systems, engineered exosomes, and combination pharmacotherapy, to both improve therapeutic efficacy and mitigate systemic toxicity. To provide insights for its safe clinical translation, this review systematically summarizes the pharmacological mechanisms, therapeutic potential, and toxicological challenges of TP in autoimmune diseases.
    Keywords:  Autoimmune Diseases; Pharmacological Mechanisms; Triptolide
    DOI:  https://doi.org/10.1142/S0192415X26500072
  46. Sci Bull (Beijing). 2026 Jan 27. pii: S2095-9273(26)00087-3. [Epub ahead of print]
      The rapid progress of interdisciplinary medicine has significantly boosted ultrasound-based therapeutic modalities and strategies. The sonosensitizers, as core components of traditional sonodynamic therapy, have drawn escalating research focus for their unique therapeutic performance, but their clinical translation remains severely hampered by critical bottlenecks of biodegradability, required semiconductor characteristic, and long-term biosafety risks, which underscore an urgent demand for innovative sonosensitizers coupled with breakthrough therapeutic modalities to revolutionize ultrasound-based therapeutics. Herein, we strategically engineered the optimized iron oxyhydroxide nanorods as a high-performance ultrasound-activated sono-tribocatalytic nanosystem for efficient sono-tribocatalytic therapy (STT). This sono-tribocatalytic sonosensitizer demonstrates exceptional tribocatalytic efficacy in radical generation while maintaining excellent recyclability. Its mechanism originates from the surface charges on sonosensitizers generated by tribocatalysis that interact with dissolved oxygen and hydroxyl species, which generate reactive oxygen species to drive redox reactions. Crucially, the accumulated cytotoxic hydroxyl and superoxide radicals induce simultaneous mitochondrial dysfunction and redox homeostasis disruption in cancer cells, triggering specific PANoptosis. The in vivo assessments validate its potent antineoplastic effect. It achieves remarkable tumor inhibition through mechano-chemical activation by the intrinsic STT mechanism. This study establishes the first STT paradigm capable of inducing PANoptosis for efficient cancer treatment, thereby significantly expanding the application scope of sonocatalytic medicine to diverse disease interventions.
    Keywords:  FeOOH; PANoptosis; Sono-tribocatalytic therapy; Sonocatalytic medicine; Tribocatalysis
    DOI:  https://doi.org/10.1016/j.scib.2026.01.061
  47. Nanomaterials (Basel). 2026 Jan 27. pii: 172. [Epub ahead of print]16(3):
      Tumor-associated macrophages (TAMs) and dendritic cells (DCs) play pivotal roles in shaping the tumor immune microenvironment, often contributing to immunosuppression and therapy resistance. Recent advances in nanotechnology have enabled precise modulation of these immune populations, offering a promising avenue to enhance the efficacy of cancer immunotherapy. Nano-enabled platforms can reprogram TAMs from a pro-tumorigenic M2-like phenotype to an anti-tumorigenic M1-like state, thereby restoring their capacity to phagocytose tumor cells and produce pro-inflammatory cytokines. Concurrently, nanomaterials can enhance DC activation and antigen presentation, promoting robust T-cell priming and adaptive immune responses. Various nanocarriers, including liposomes, polymeric nanoparticles, and inorganic nanostructures, have been engineered to deliver immune modulators, nucleic acids, or tumor antigens selectively to TAMs and DCs within the tumor microenvironment. These strategies have demonstrated synergistic effects when combined with immune checkpoint blockade or cytokine therapy, resulting in improved tumor regression and long-term immunological memory in preclinical models. Despite these promising outcomes, challenges remain regarding nanomaterial biocompatibility, targeted delivery efficiency, and potential off-target immune activation. Ongoing research is focused on optimizing nanoparticle physicochemical properties, surface functionalization, and multi-modal delivery systems to overcome these limitations. This review highlights recent advances in nano-enabled modulation of TAMs and DCs, emphasizing mechanistic insights, therapeutic outcomes, and translational potential. By integrating nanotechnology with immunotherapy, these approaches offer a powerful strategy to overcome tumor immune evasion, paving the way for more effective and personalized cancer treatments.
    Keywords:  M2-like phenotype; T-cell priming; dendritic cells; nanoparticle; tumor microenvironment; tumor-associated macrophages
    DOI:  https://doi.org/10.3390/nano16030172
  48. Mater Today Bio. 2026 Feb;36 102746
      The escalating threat of antimicrobial resistance (AMR) necessitates urgent development of novel antibacterial agents. Photodynamic therapy (PDT) emerges as a promising alternative strategy due to its non-invasiveness and low resistance development risk. And natural products provide ideal scaffolds for photosensitizer (PS) design owing to inherent bioactivity and biocompatibility. Herein, we reported a structurally modified natural products derived aggregation-induced emission photosensitizer (BioAIE-PS), TPA-CRY, engineered from the natural alkaloid cryptolepine (CRY) for combating bacterial infections and biofilms. This molecular redesign successfully overcame the detrimental aggregation-caused quenching (ACQ) effect and weak reactive oxygen species (ROS) generation intrinsic to native CRY. Notably, upon photoexcitation, TPA-CRY demonstrated substantially enhanced ROS production and superior in vitro antibacterial efficacy compared to its parent compound CRY. Furthermore, it exhibited potent activity against both bacterial biofilms and persister cells. Mechanistic investigations elucidated that bacterial eradication occurs through disruption of membrane integrity, leakage of cellular contents, and ROS-mediated oxidative damage. Crucially, significant in vivo therapeutic efficacy was validated in a murine wound infection model. This work not only validates the substantial potential of TPA-CRY in photodynamic antibacterial therapy but also provides compelling evidence for the rational development of BioAIE-PSs via structural modification of ACQ-type natural products.
    Keywords:  Aggregation-induced emission; Antibacterial activity; Biofilm; Cryptolepine; Photodynamic therapy; Reactive oxygen species
    DOI:  https://doi.org/10.1016/j.mtbio.2025.102746
  49. Ann Med Surg (Lond). 2026 Feb;88(2): 2124-2125
      Extracellular vesicles (EVs), particularly exosomes, have emerged as key mediators of intercellular communication by transporting microRNAs (miRNAs). Recent studies indicate that EV-associated miRNAs regulate gene expression across diverse physiological and pathological processes, including cancer metastasis, neuroinflammation, kidney injury, and cardiovascular disease. Understanding the selective packaging, trafficking, and functional consequences of EV-miRNA transfer may enable the development of biomarkers and targeted therapies based on vesicle-mediated signaling.
    Keywords:  biomarkers; exosomes; extracellular vesicles; intercellular communication; microRNA; precision medicine
    DOI:  https://doi.org/10.1097/MS9.0000000000004579
  50. J Control Release. 2026 Feb 09. pii: S0168-3659(26)00101-X. [Epub ahead of print]392 114699
      Polymeric nanoparticles (NPs) are a versatile delivery platform for non-viral genetic therapies. However, a key shortcoming of polymeric NPs (and other non-viral delivery vehicles) is the often-high accumulation of NPs within the liver and the spleen after systemic intravenous (IV) administration in vivo. This phenomenon is largely the result of the mononuclear phagocytic system (MPS), a class of phagocytic cells responsible for native immune response and toxin clearance within the body. One strategy to overcome NP clearance by the MPS is the use of phagocytic modulating pre-treatments to intentionally and temporarily alter the phagocytic behavior of macrophages such that sequentially administered therapeutic NPs can be delivered to extrahepatic and extrasplenic tissues. Here, we explore the use cargo-free poly(lactic-co-glycolic acid) (PLGA) "decoy" NPs as pre-treatments for phagocytic evasion of sequentially administered therapeutic NPs. Analysis via flow cytometry and fluorescence microscopy reveal that cargo-free PLGA NPs significantly decrease uptake of subsequently administered therapeutic NPs by macrophages. Specifically, we conclude that variables such as size, surfactant composition, and timing of pre-treatment influence the behavior of cargo-free PLGA decoy NPs in modulating phagocytic activity of macrophages. In in vivo studies, we report decreased accumulation in the liver and increased deposition of therapeutic NPs in the lung with pre-administration of cargo-free decoy PLGA NPs. Together, these studies suggest pre-treatment with decoy NPs can reduce therapeutic NP clearance, with the potential to improve nanomedicine delivery capabilities for a wide range of therapeutics and disease targets.
    Keywords:  Drug delivery; Gene delivery; Mononuclear phagocytic system; Nanoparticles
    DOI:  https://doi.org/10.1016/j.jconrel.2026.114699
  51. Front Immunol. 2026 ;17 1701440
      Sepsis-induced acute lung injury (S-ALI) represents a life-threatening condition with complex molecular pathophysiology and limited therapeutic options. Emerging evidence highlights the critical role of competing endogenous RNA (ceRNA) networks, particularly long non-coding RNA (lncRNA)-microRNA (miRNA)-mRNA axes, in orchestrating cell type-specific responses during S-ALI. This review synthesizes recent advances illustrating how these regulatory circuits modulate alveolar epithelial apoptosis, endothelial permeability, macrophage polarization, and neutrophil infiltration, thereby driving inflammation, barrier dysfunction, and immune dysregulation. Furthermore, we explore the promising therapeutic potential of engineered extracellular vesicles for targeted delivery of ceRNA components-such as miRNA mimics or lncRNA inhibitors-to precisely manipulate these networks. Despite progress, significant challenges remain, including model translatability, functional redundancy, and delivery efficiency. Overcoming these hurdles may unlock novel strategies for treating S-ALI, moving toward personalized and context-specific interventions.
    Keywords:  cell-specific regulation; competing endogenous RNA; extracellular vesicles; lncRNA-miRNA-mRNA axis; sepsis-associated acute lung injury
    DOI:  https://doi.org/10.3389/fimmu.2026.1701440
  52. Small Methods. 2026 Feb 12. e01731
      Macrophage membrane-coated nanoparticles (M2M-NPs) offer a promising strategy for targeting immunologically "cold" tumors resistant to conventional therapies. However, workflows for membrane isolation and NP coating remain limited and often lack reproducibility. Herein, a multi-step process was established for isolating plasma membranes from human M2-like macrophages. This optimized workflow combines hypotonic lysis, Dounce homogenization, and differential centrifugation, yielding M2M fractions with consistent protein, lipid, and DNA profiles. Building on this process, a detailed and reproducible method for preparing membrane-derived nanovesicles (M2M-NVs) was developed, and these nanovesicles were thoroughly characterized in terms of morphology, particle size, and stability under various short-term storage conditions. The incorporation of fluorescent lipids and cholesterol was essential for efficient extrusion and enhanced nanovesicle stability. To systematically evaluate the influence of nanocore dynamics and hydrophobicity on M2M coating efficiency, different model nanocores (TPGS micelles, VD3 micelles, and PLGA NPs) were employed. Among these, semi-rigid hydrophobic PLGA NPs produced the most uniform and stable coatings. Furthermore, PLGA/M2M-NPs loaded with paclitaxel demonstrated high colloidal stability, excellent hemocompatibility, enhanced immune evasion, and selective cytotoxicity against triple-negative breast cancer, pancreatic, and glioblastoma cells compared with free paclitaxel and the clinical approved nanoformulation (Abraxane). Collectively, this reproducible workflow offers a reliable foundation for engineering macrophage membrane-based biomimetic NPs and advances their translational potential for treating immunologically "cold" tumors.
    Keywords:  bioinspired drug delivery; cell membrane isolation; homotypic targeting; macrophage membrane‐coated nanoparticles; nanocore screening
    DOI:  https://doi.org/10.1002/smtd.202501731
  53. bioRxiv. 2026 Feb 07. pii: 2026.02.04.703875. [Epub ahead of print]
      Achieving tumor-specific delivery and sustained activation of both cytotoxic and immune-modulating agents remains a critical challenge in chemoimmunotherapy. Here, we present a bacterial platform engineered to combine enzyme/prodrug chemotherapy with immunotherapy, where tumor-homing E. coli Nissle 1917 expresses cytosine deaminase to convert the prodrug 5-fluorocytosine into the cytotoxic drug 5-fluorouracil within tumors. Concurrently, the engineered bacteria produce an IL-15 superagonist and a PD-L1 blocking nanobody to mitigate the immunosuppressive effects of tumor-localized chemotherapy. This platform demonstrated potent antitumor effects in the murine MC38 solid tumor model. Mechanistic studies showed that the combination therapy enhances activation of antigen-presenting cells, T cells and natural killer cells, while reducing immunosuppressive populations. In summary, our approach integrates enzyme/prodrug therapy and immunotherapy into a single bacterial delivery system, overcoming the limitations of conventional therapies and offering a scalable and precision-engineered strategy with an improved safety profile for synergistic cancer treatment.
    DOI:  https://doi.org/10.64898/2026.02.04.703875
  54. Ann Med Surg (Lond). 2026 Feb;88(2): 1437-1440
      Rhinoplasty often requires cartilage grafts to restore nasal contour and function. Traditional options, such as autologous, allogeneic, and synthetic materials, remain limited by donor-site morbidity, restricted availability, and long-term complications, including resorption and extrusion. Advances in tissue engineering and biomaterial science have led to the development of smart artificial cartilage implants that combine mechanical strength with biologic responsiveness. These materials can adapt to external stimuli, such as mechanical load, temperature, or electrical signals, promoting better integration and durability. Hydrogels, piezoelectric composites, and nanohybrid scaffolds have shown enhanced chondrogenic potential and mechanical compatibility in preclinical studies. Furthermore, three-dimensional bioprinting and stem-cell-based strategies enable the fabrication of patient-specific constructs that reduce intraoperative manipulation and improve anatomical fit. Although early experimental and limited clinical results are promising, current evidence remains heterogeneous and largely confined to small case series. Broader clinical validation, standardized testing protocols, and clear regulatory frameworks are needed to ensure safe and reproducible translation. Smart artificial cartilage implants thus represent a significant step toward next-generation rhinoplasty materials, merging functional durability with biologic adaptability.
    Keywords:  3D bioprinting; artificial cartilage implants; biomaterials; rhinoplasty; smart materials; tissue engineering; tissue regeneration
    DOI:  https://doi.org/10.1097/MS9.0000000000004461
  55. Front Cell Dev Biol. 2026 ;14 1788590
      
    Keywords:  endometrium; human reproduction; implantation; infertility; recurrent implantation failure; uterine NK cells
    DOI:  https://doi.org/10.3389/fcell.2026.1788590
  56. Front Neurol. 2025 ;16 1665405
      Traumatic brain injury (TBI) unfolds through a well-defined chronology-hyperacute excitotoxic and inflammasome bursts, acute apoptotic and blood-brain-barrier failure, and subacute neurovascular remodeling-that no single-pathway drug can adequately cover. Recombinant erythropoietin (EPO) limits secondary damage in animals, yet its erythropoietic drive and thrombotic liability have stalled clinical adoption. This review integrates structural biology, pharmacology and translational data on four engineered EPO derivatives-carbamylated EPO, asialo-EPO, darbepoetin alfa and the helix-B surface peptide (HBSP/cibinetide)-that decouple cytoprotection from red-cell stimulation. We first outline how specific modifications (carbamylation, desialylation, hyper-glycosylation or helix truncation) bias EPOR signaling toward PI3K-AKT and away from JAK2-STAT5. We then match each derivative to its optimal injury window. Meta-analyses of randomized trials suggest a possible trend toward lower short-term mortality without a consistent functional benefit or thrombotic signal. By integrating molecular mechanisms, experimental findings, and early clinical observations, this review outlines hypotheses and future trial frameworks for phase-targeted, erythropoietin-based neuroprotection. Further controlled studies are required to establish safety, efficacy, and optimal therapeutic timing before translation to routine clinical use.
    Keywords:  erythropoietin derivatives; neuroprotection; protein engineering; secondary injury phases; traumatic brain injury
    DOI:  https://doi.org/10.3389/fneur.2025.1665405
  57. Plant Cell Environ. 2026 Feb 08.
      Heat stress is a major abiotic stress that limits alfalfa (Medicago sativa L.) productivity. To test whether cytokinin-overexpressing engineered rhizobia could enhance heat tolerance, we inoculated alfalfa with modified rhizobia and evaluated their physiological and molecular responses. We found that inoculation with engineered rhizobia significantly increased trans-Zeatin content in alfalfa. Compared with control rhizobia-inoculated plants, engineered rhizobia-inoculated plants exhibited increased plant height, fresh/dry weight, relative water content, and photosynthetic efficiency (total chlorophyll and carotenoids), alongside reduced hydrogen peroxide (H₂O₂) and superoxide (O₂.-) levels under heat stress. RNA-seq analysis revealed that engineered rhizobia upregulated heat stress-responsive genes in alfalfa, which was further verified by qRT-PCR. Metabolomics analyses showed significant alterations in phenylpropanoid, flavonoid, phenolic acid, and salicylic acid metabolic pathways in engineered rhizobia-inoculated plants under heat stress. Contrary to conventional approaches, our results demonstrate that cytokinin-overexpressing rhizobia not only enhance alfalfa heat tolerance but also activate multi-pathway stress responses. Collectively, these findings propose a novel strategy for developing heat-tolerant alfalfa through engineered rhizobia-mediated cytokinin biosynthesis, which helps to promote the development of sustainable alfalfa breeding for heat-tolerant varieties.
    Keywords:  alfalfa; cytokinin; engineered rhizobia; heat stress; transcription regulation
    DOI:  https://doi.org/10.1111/pce.70396
  58. Sci Rep. 2026 Feb 10.
      Targeting cellular senescence presents a promising approach to slow visible skin aging and promote tissue repair. However, most preclinical models fail to capture the full architecture of human skin or accommodate diverse skin types, limiting their translational relevance. To address this gap, we developed a controlled ex vivo human skin explant platform using freshly acquired tissues from donors of varying ages and Fitzpatrick skin types. This model applies standardized UVA and UVB doses to induce reproducible photodamage, enabling the assessment of both preventative and reparative effects of topical treatments. The results showed that ND-ZnO and NAC reduced levels of p16^INK4a and p53, which are key biomarkers measuring cellular senescence; ND-ZnO and exosomes lowered IL-1β expression, which is a biomarker measuring inflammation. Histological analysis confirmed these findings, with ND-ZnO-treated skins preserved epidermal structure, reduced inflammatory features, and maintained dermal collagen organization. We then conducted a four-week single-patient case study using the same ND-ZnO formulation. Visible improvements in redness, pigmentation, and texture were observed, aligned with the molecular and histological changes seen ex vivo. These findings suggested that the ex vivo platform has the potential to be used as a more inclusive, human-relavent model for evaluating and quantifying the anti-aging efficacies of topical treatments across diverse skin types and age groups.
    Keywords:  Aging biomarkers; Cellular senescence; Ex vivo skin explants; Multiethnic skin model; Skin aging
    DOI:  https://doi.org/10.1038/s41598-026-38877-x
  59. Immunity. 2026 Feb 10. pii: S1074-7613(26)00042-7. [Epub ahead of print]59(2): 235-237
      Immunotherapeutic approaches to brain aging remain largely preclinical and in early translational stages, and they have focused mostly on modulating innate immunity. In this issue of Immunity, Negredo et al. identify T cells bearing exhaustion-like signatures as a hallmark of brain aging and reveal the beneficial effects of an engineered IL-10 variant that functionally uncouples pro- and anti-inflammatory signaling in microglia.
    DOI:  https://doi.org/10.1016/j.immuni.2026.01.021
  60. Oncol Rep. 2026 Apr;pii: 68. [Epub ahead of print]55(4):
      The poor prognosis and high mortality rate of non‑small cell lung cancer are largely driven by its aggressive migratory and invasive behavior. Epithelial‑mesenchymal transition (EMT) is a central mechanism conferring these malignant traits. The present study examined the expression profile of the sodium channel β4 subunit (SCN4B) in lung adenocarcinoma (LUAD) and explored its regulatory role in EMT. Transcriptomic data from The Cancer Genome Atlas were analyzed to compare SCN4B expression between LUAD and normal tissues, and to assess its relationship with TNM clinical stage (I‑IV), overall survival and diagnostic performance using non‑parametric tests, Kaplan‑Meier analysis and receiver operating characteristic curves, respectively. Functional enrichment analysis, including Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, and immune cell infiltration profiling were performed on SCN4B‑associated differentially expressed genes. In vitro, the A549 and H1299 LUAD cell lines were engineered to overexpress SCN4B. Viability, migration, invasion and apoptosis were evaluated using Cell Counting Kit‑8 assays, wound healing assays, Transwell assays and flow cytometry. In addition, western blotting was conducted to assess EMT markers, including E‑cadherin, N‑cadherin, Vimentin and Snail. The results demonstrated that SCN4B expression was markedly reduced in LUAD tissues and low SCN4B expression was associated with unfavorable clinical outcomes. KEGG analysis revealed enrichment of SCN4B‑related genes in the 'cell adhesion molecules' pathway, and SCN4B expression levels differed markedly between TNM tumor (T) pathologic stages T1 and T2. Furthermore, SCN4B overexpression suppressed viability, migration and invasion of A549 and H1299 cells, while promoting apoptosis. Western blotting demonstrated upregulation of E‑cadherin, and downregulation of N‑cadherin, Vimentin and Snail in the SCN4B overexpression group compared with the empty vector group, indicating inhibition of EMT. In conclusion, low SCN4B expression was associated with poor prognosis in LUAD. Notably, restoring SCN4B levels suppressed LUAD cell viability, migration and invasion in vitro, accompanied by inhibition of EMT. These findings highlighted SCN4B as a potential tumor suppressor and a promising therapeutic target for LUAD.
    Keywords:  The Cancer Genome Atlas; epithelial‑mesenchymal transition; invasion; lung adenocarcinoma; migration; sodium channel β4 subunit
    DOI:  https://doi.org/10.3892/or.2026.9073
  61. Biotechnol Bioeng. 2026 Feb 12.
      Spinal cord injury (SCI) initiates a cascade of secondary pathological events largely driven by neuroinflammation, where microglial polarization plays a pivotal role. Modulating microglial polarization from M1 to M2 phenotype has emerged as a promising therapeutic strategy. Fibroblast growth factor 21 (FGF21) is known to regulate inflammatory responses, but its delivery to the injury site remains challenging. In this study, we engineered a biocompatible hyaluronic acid (HA) hydrogel capable of sustained release of mesenchymal stem cell-derived exosomes enriched with FGF21 (MSCs-Exo-FGF21). The hydrogel's physicochemical properties and release kinetics were characterized, and its cytocompatibility was verified in vitro. LPS-stimulated microglial cells were used to evaluate polarization, cytokine profiles, and activation of the STAT3/SOCS3 signaling pathway. A rat SCI model was used to assess neuroprotection and functional recovery. MSCs-Exo-FGF21 promoted M2 polarization of microglia, suppressed M1 markers, and significantly activated the STAT3/SOCS3 pathway both in vitro and in vivo. ELISA and qPCR analyses revealed reduced proinflammatory cytokines (IL-1β, TNF-α) levels and elevated anti-inflammatory IL-10. In SCI rats, hydrogel-mediated delivery of MSCs-Exo-FGF21 reduced lesion cavity size, preserved neuronal structure, and significantly improved hindlimb locomotor function. The hydrogel provided a favorable microenvironment for sustained exosome release and cellular uptake. Our findings demonstrate that hydrogel-based delivery of MSCs-Exo-FGF21 effectively reprograms microglial polarization through STAT3/SOCS3 signaling, alleviates neuroinflammation, and promotes functional recovery after SCI. This exosome-hydrogel platform offers a promising therapeutic avenue for modulating immune responses and enhancing neural repair in central nervous system (CNS) trauma.
    Keywords:  exosomes derived from mesenchymal stem cells (MSC‐Exo); fibroblast growth factor 21 (FGF21); hyaluronic acid (HA) hydrogel; spinal cord injury (SCI)
    DOI:  https://doi.org/10.1002/bit.70165
  62. Mol Ther Oncol. 2026 Mar 19. 34(1): 201132
      Oncolytic virotherapy (OV) has emerged as a promising cancer treatment strategy, utilizing viruses to selectively infect and destroy tumor cells while simultaneously stimulating anti-tumor immunity. OV has also been shown to modulate the tumor immune microenvironment, enhancing the efficacy of immunotherapy. Despite the recent regulatory approvals of oncolytic viruses such as T-VEC (JS1/34.5-/47-/GM-CSF), Oncorine (H101), and Teserpaturev (G47Δ), the clinical impact of OV remains limited by its reliance on intratumoral administration. Systemic delivery is essential for effectively treating metastatic and inaccessible tumors but is hindered by two major challenges: rapid clearance by the mononuclear phagocyte system (MPS) and neutralization by antiviral antibodies. To overcome these barriers, we developed FusOn-SD, an enhanced version of FusOn-H2 engineered for systemic delivery. Our strategy integrates both genetic and adaptive modifications: (1) incorporating the extracellular domain (ECD) of CD47 to evade MPS-mediated clearance and (2) serially passaging the virus in immune sera to enhance resistance to neutralizing antibodies. Preclinical studies demonstrate that FusOn-SD efficiently reaches tumor sites following systemic administration, exhibiting enhanced immune evasion and oncolytic potency. These findings position FusOn-SD as a promising candidate for advancing OV beyond localized injections, with the potential to transform virotherapy into a viable treatment for metastatic cancer.
    Keywords:  CD47; herpes simplex virus; oncolytic virus; systemic delivery; virotherapy
    DOI:  https://doi.org/10.1016/j.omton.2026.201132
  63. Bioact Mater. 2026 Apr;58 701-718
      The increasing prevalence and incidence urge efficient treatment of osteoarthritis (OA). In contrast, a single modality is hard to combat OA's complicated pathogenesis and achieve comprehensive chondroprotective function. Through RNA sequencing, we identified bone marrow mesenchymal stromal cell-derived exosomes (BMSC-Exo) and cartilage progenitor cell-derived exosomes (CPC-Exo) have distinct enrichment of miRNA contents, emphasizing macrophage and chondrocyte modulation, respectively. Thus, inspiring us to develop a bi-exosome combination strategy, which combines anti-inflammatory BMSC-Exo and anti-catabolic CPC-Exo, to alleviate osteoarthritis progression via simultaneous regulation of macrophage polarization and chondrocyte phenotype. Once delivered into the rat knee joint cavity by hyaluronic acid methacryloyl microspheres, the bi-exosome combination remarkably postponed OA progression via combating the joint inflammatory and catabolic environment, in which the dominant interventive pathways (i.e., miR-708-5p/NRP-1, miR-431/BRCA-1/PLK-1, and miR-7a-5p/NOTCH-3) were further revealed. This work presents the tailoring of exosome compositions to modulate multitargeting, thereby creating a potential for OA treatment.
    Keywords:  Bi-exosome; Cartilage regeneration; Combinatorial effects; Microsphere; miRNA
    DOI:  https://doi.org/10.1016/j.bioactmat.2025.11.050
  64. J Agric Food Chem. 2026 Feb 09.
      Thiamine (Vitamin B1), an essential water-soluble vitamin, is composed of a pyrimidine and a thiazole ring. Owing to its functional roles as a coenzyme and its anti-inflammatory and antioxidant properties, it plays a critical role in disease prevention and therapeutic interventions. Currently, industrial production of thiamine relies primarily on chemical synthesis-a process that generates significant amounts of hazardous waste and byproducts. In contrast, microbial biosynthesis represents a more sustainable and environmentally friendly alternative. This review first outlines thiamine metabolism in microorganisms, highlighting ThiC as the key rate-limiting enzyme in its biosynthesis. It then summarizes potential strategies for improving thiamine biomanufacturing, and proposes that optimizing metabolic flux together with energy and cofactor balance at critical nodal points is essential for overcoming current yield limitations. Finally, to overcome specific bottlenecks in thiamine biosynthesis, such as precursor transport and pathway optimization, we propose that transport engineering and gene mining represent promising strategies complementary to recent advances in enzyme-directed evolution and metabolic engineering.
    Keywords:  ThiC; de novo synthesis; engineered strains; thiamine
    DOI:  https://doi.org/10.1021/acs.jafc.5c12462