bims-engexo Biomed News
on Engineered exosomes
Issue of 2025–10–26
ten papers selected by
Ravindran Jaganathan, Universiti Kuala Lumpur



  1. Extracell Vesicles Circ Nucl Acids. 2025 ;6(3): 475-503
      Exosomes, as key mediators of intercellular communication, have shown great potential in disease intervention and therapy in recent years. As natural nanocarriers, exosomes play a crucial role in transporting a wide array of cargo. Among these, miRNAs carried by exosomes are pivotal in gene regulation and the modulation of cellular signaling. Given that miRNAs are essential gene regulators, understanding how miRNAs are selectively loaded into exosomes is crucial for the development of novel diagnostic and therapeutic approaches. This review provides a detailed overview of the biogenesis and secretion mechanisms of exosomes, with a particular focus on the molecular mechanisms governing miRNA sorting into exosomes. Specifically, it highlights the miRNA motifs associated with exosomes enrichment (EXOmotifs), as well as those related to intracellular miRNA enrichment (CELLmotifs), along with RNA-binding proteins (RBPs) involved in sorting. We summarize the current progress in this field and discuss strategies for engineering Exosomes - such as gene editing, drug loading, and surface modification - to enhance their functionality and specificity. By exploring these mechanisms, this review offers a theoretical foundation for the application of engineered exosomes in disease treatment and outlines future research directions and potential applications.
    Keywords:  CELLmotifs; EXOmotifs; Extracellular vesicles; RNA-binding proteins; engineered extracellular vesicles; microRNA sorting
    DOI:  https://doi.org/10.20517/evcna.2025.47
  2. Mater Today Bio. 2025 Oct;34 102166
      To enhance treatment outcomes for nasopharyngeal carcinoma (NPC), this study evaluates the efficacy of tumor mitochondrial protein 1 (TMTP1)-modified extracellular vesicles (EVs) for targeted ropivacaine delivery. The limited efficacy of conventional therapies in NPC highlights the need for innovative strategies that can address both tumor cell proliferation and pain management. EVs, isolated from NPC cell lines and modified with TMTP1 for enhanced tumor targeting, were loaded with ropivacaine to investigate their effects on tumor suppression and immune modulation. Through in vitro assessments, including CCK-8 and Hoechst assays, R-TMTP1 EVs showed effectively inhibited tumor growth and enhanced drug cytotoxicity. Further investigations revealed that these EVs suppress Cyclin B1 (CCNB1) expression and disrupt autophagic processes, enhancing apoptosis. In vivo studies using mouse models demonstrated that R-TMTP1 EVs effectively localize to tumor sites, significantly reducing tumor growth and alleviating pain, verified by enhanced T cell activity. These promising results advocate for the further exploration of R-TMTP1 EVs as a dual-function therapeutic tool in NPC.
    Keywords:  Immune evasion; Nasopharyngeal carcinoma; Ropivacaine; TMTP1 peptide; Tumor extracellular vesicles
    DOI:  https://doi.org/10.1016/j.mtbio.2025.102166
  3. Curr Pharm Des. 2025 Oct 17.
       INTRODUCTION: Hepatocellular carcinoma (HCC) is the third leading cause of cancer deaths globally. Traditional treatments face limitations like low effectiveness, poor specificity, and significant side effects. Gene therapy, particularly siRNA-based, is promising for targeted gene regulation but requires effective delivery systems due to the instability and poor target delivery of unmodified siRNA.
    METHODS: This study examined the storage and biological stability of LP-PEI-SPION (LPS) and GPC3-LPPEI- SPION (GLPS). The potential of these agents as tumor imaging contrast agents and the targeting ability of gene delivery carriers were assessed through ex vivo organ fluorescence imaging and in vivo tumor magnetic resonance imaging (MRI). Antitumor efficacy was evaluated through tumor volume, protein blotting, immunohistochemistry, and TUNEL assays. In vivo safety was evaluated using HE staining, nude mouse weight changes, and blood biochemical indicators.
    RESULTS: LPS and GLPS both formed stable siRNA complexes. GLPS showed excellent tumor targeting in vivo. MRI results showed that the GPC3-targeting peptide effectively enhanced the MR imaging performance and diagnostic accuracy. Tumor volume and weight measurements demonstrated potent tumor inhibition by GLPS/siRNA. Immunoblotting and immunohistochemistry revealed significant GPC3 reduction in the GLPS/ siRNA-targeted group. Safety evaluations confirmed good biocompatibility for both LPS/siRNA and GLPS/ siRNA.
    CONCLUSION: GLPS/siRNA demonstrates good stability, tumor targeting, imaging capability, and antitumor efficacy with favorable safety, positioning it as a promising theragnostic platform for HCC. This integrated system provides novel clinical tools for diagnosis and treatment, establishes a foundation for clinical translation, and enables simultaneous tumor imaging and gene therapy-offering innovative strategies for combined tumor theranostics.
    Keywords:  GPC3.; siRNA; superparamagnetic iron oxide nanoparticles; targeted therapy
    DOI:  https://doi.org/10.2174/0113816128395585250923122829
  4. Zhen Ci Yan Jiu. 2025 Oct 25. pii: 1000-0607(2025)10-1114-10. [Epub ahead of print]50(10): 1114-1123
       OBJECTIVES: To observe the effect of electroacupuncture (EA) on knee function and symptoms, intestinal flora and TLR4/MyD88/NF-κB signaling pathway of articular cartilage in rabbits with knee osteoarthritis (KOA), so as to explore its potential mechanism underlying improvement of knee function by regulating the gut-joint axis response of KOA.
    METHODS: Thirty-two Japanese white rabbits were randomly divided into blank, model, glucosamine and EA groups, with 8 rabbits in each group. The KOA model was reproduced by using modified Hulth method. The rabbits in the EA group were given EA (2 Hz/100 Hz, 0.5-1.5 mA) at bilateral "Xuehai"(SP10), "Yinlingquan"(SP9) and "Dubi"(ST35) for 15 min, once daily, 5 times a week for 4 weeks. The rabbits of the glucosamine group received glucosamine solution once daily, 5 times a week for 4 weeks. The knee function was evaluated by Lequesne MG index of severity for osteoarthritis (total scores of pain, swelling, range of motion, and gait) after modeling and treatment. H.E. staining was used to observe the histopathological changes of the knee cartilage tissue. Immunofluorescence histochemical method was used to detect the expressions of MyD88 and NF-κB p65, and Wes automated protein blot quantitative analysis technique was employed to detect the protein expressions of TLR4, MyD88 and NF-κB p65 in the knee cartilage tissue. Analysis of the species structure changes of intestinal flora was detected by 16S rDNA high-throughput sequencing.
    RESULTS: After modeling, compared with the blank group, the Lequesne MG score, immunofluorescence intensity of MyD88 and NF-κB p65, and the protein expression levels of TLR4, MyD88 and NF-κB p65 were significantly increased in the model group (P<0.05). H.E. staining showed thin and rough surface of the knee cartilage, clusters and disordered arrangement of chondrocytes, a few cellular nuclei being dark blue-purple in staining, with some nuclei being shrank, ruptured, and disappeared in the model group. In comparison with the model group, the Lequesne MG score, fluorescence intensity of MyD88 and NF-κB p65, and the protein expression levels of TLR4, MyD88 and NF-κB p65 were significantly decreased in both EA and glucosamine groups (P<0.05). The effects of EA were significantly superior to glucosamine in down-regulating the protein expression levels of TLR4, MyD88 and NF-κB (P<0.05). H.E. staining showed relatively complete surface of the knee cartilage, slightly hypertrophic chondrocytes with relatively clear nucleus and relatively complete tide line in both EA and glucosamine groups. Results of 16S rDNA sequencing showed that compared with the blank group, the Shannon index was obviously increased (P<0.05), the relative abundance of Proteobacteria, Actinobacteria, Escherichia coli-Shigella and Clostridium UCG-014 was elevated, and the relative abundance of Firmicutes, Verrucomicrobia, Comamonas and Acmea bacteria was decreased in the model group. In comparison with the model group, the Chao1 index and Shannon index were increased (P<0.05), the relative abundance of Proteobacteria, Actinobacteria and Escherichia coli-Shigella was decreased, while the relative abundance of Firmicutes, Comamonas and Nobilus was significantly increased in both EA and glucosamine groups.
    CONCLUSIONS: EA can significantly improve the symptoms and function of knee joint in KOA rabbits, which may be associated with its functions in inhibiting cartilage injury and inflammation reaction by regulating TLR4/MyD88/NF-κB signaling pathway and intestinal flora diversity through the "gut-joint" axis.
    Keywords:  Electroacupuncture; Inflammation; Intestinal flora; Knee osteoarthritis; TLR4/MyD88/NF- κB signaling pathway
    DOI:  https://doi.org/10.13702/j.1000-0607.20240990
  5. Adv Healthc Mater. 2025 Oct 20. e03453
      Type 1 diabetes mellitus (T1DM) is a chronic autoimmune disorder characterized by autoimmune-mediated destruction of pancreatic β-cells through cytotoxic T lymphocyte infiltration, leading to absolute insulin deficiency. Supplementation of exogenous insulin can't protect remaining β-cells or address the root autoimmune cause. The emerging therapeutic strategies focus on immunomodulatory approaches, targeting the activation of the programmed death 1/programmed death ligand 1 (PD-1/PD-L1) pathway could attenuate T cell-mediated β-cell destruction, thereby alleviating inflammation in early-stage T1DM. However, nonselective PD-1/PD-L1 blockade can cause toxicity. Herein, exosomes from PD-L1high MCF-7 cells are utilized, modified with monocyte-targeting IgG, and have their contents removed via electroporation to eliminate tumorigenicity. Monocytes have the characteristic of targeting inflammatory sites. rExo-IgG is stably anchored to the monocytes' membrane through IgG and transported as a backpack of monocytes to the inflammatory sites (pancreas and wounds). In the pancreatic tissue, rExo-IgG through PD-1/PD-L1 pathway, inhibiting their activation and protecting β-cells. At the site of tissue injury, rExo-IgG repolarizes macrophages from pro-inflammatory M1 to anti-inflammatory M2. It also promotes fibroblast proliferation and migration, enhancing tissue regeneration. This dual-targeting exosome platform not only exhibits therapeutic efficacy against early-stage T1DM but also offers a novel strategy for the treatment of diabetic wound healing disorders.
    Keywords:  backpack; exosome; monocyte; type 1 diabetes; wound healing
    DOI:  https://doi.org/10.1002/adhm.202503453
  6. Gene. 2025 Oct 18. pii: S0378-1119(25)00631-6. [Epub ahead of print] 149842
       BACKGROUND: Doxorubicin-induced cardiomyopathy (DCM) remains a major clinical challenge, highlighting the need for early diagnostic biomarkers. Exosomal miRNAs have emerged as promising candidates because of their stability and regulatory roles in cardiovascular diseases.
    METHODS: Exosomes were isolated from myocardial tissue samples of DOX-treated and control rats using differential ultracentrifugation and were subsequently characterized by transmission electron microscopy (TEM), Western blotting, and nanoparticle tracking analysis (NTA). Differentially expressed miRNAs were screened by microarray analysis. The miRanda algorithm was used to predict target genes, followed by functional enrichment analysis. qRT‒PCR validated selected miRNAs and their target genes.
    RESULTS: Doxorubicin administration induced significant cardiac dysfunction, characterized by decreased left ventricular ejection fraction (LVEF) and increased serum levels of cardiac biomarkers (cTnI, BNP, and CK-MB). Microarray profiling revealed 26 differentially expressed miRNAs, and KEGG enrichment analysis indicated enrichment in the MAPK signaling pathway. qRT‒PCR demonstrated upregulation of exosomal miR-182 and downregulation of Taok2 mRNA, a key MAPK gene. ROC analysis indicated the potential of exosomal miR-182 for DCM diagnosis.
    CONCLUSION: Exosomal miR-182 may serve as a diagnostic marker for DCM. Bioinformatic analyses predict its potential regulation of the MAPK pathway through Taok2 targeting, although this mechanistic relationship requires experimental validation. These findings provide new perspectives for the early monitoring of DCM.
    Keywords:  Cardio-oncology; Doxorubicin-induced cardiomyopathy; Myocardium-Derived Exosomal miRNAs; Taok2; miR-182
    DOI:  https://doi.org/10.1016/j.gene.2025.149842
  7. J Orthop Surg Res. 2025 Oct 21. 20(1): 911
      Tendon injury is one of the most frequently encountered soft tissue injuries with slow repair and poor functional recovery. Over the past few years, there's been a buzz about how exosomes might boost tissue repair and regeneration. This research dive delves into the question of whether Schwann cell-derived exosomes (SCDEs) can jumpstart tendon healing by tweaking the PTEN/PI3K/Akt signaling chain.been concentrated on the effects of exosomes in promoting tissue regeneration and repair. In the present study, we would like to explore whether exosomes derived from Schwann cells (SCDE) could promote tendon repair via modulation of PTEN/PI3K/Akt signaling cascade. This study integrates experiments performed both in vitro and in vivo. Tendon cells were categorized into the NC and SCDE groups, with a scratch assay employed.vitro and in vivo conditions tendo cells were divided into the NC group and SCDE group, and scratch assay, Transwell migration assay, flow cytometry for cell cycle detection, and Western blot and qRT-PCR analyses were performed to measure SCX, DCN, COL1A1, p-AKT, PTEN, and other markers.In the in vivo experiments, a rat model of 1/3 patellar tendon defect was established, and hydrogel or hydrogel + SCDE was injected. Tissues were gathered at 2, 4, and 8 weeks following the surgical procedure, and HE, Masson, and Sirius Red stains were applied to gauge the healing process. Important protein levels were assessed at the 2 week mark after the operation.Masson, and Sirius Red staining were performed to evaluate tissue repair. Key protein expression was measured at 2 weeks post-surgery.
    DOI:  https://doi.org/10.1186/s13018-025-06352-4
  8. Dev Neurobiol. 2025 Oct;85(4): e23010
      Hypoxia-induced neonatal seizures (HINSs) are a major cause of long-term cognitive deficits and heightened epilepsy risk in adulthood. Early inflammatory responses following HINS contribute to these pathological outcomes. This study examined the sustained neuroprotective benefits of exosomes derived from mesenchymal stem cells (MSC-exosomes) in a rat model of HINS, leveraging their anti-inflammatory and neuroregenerative properties. Forty-nine male and female Wistar rats were divided into four groups: (1) control + saline, (2) control + exosome, (3) hypoxia + saline, and (4) hypoxia + exosome. Neonatal rats (postnatal day 10) were subjected to hypoxia (5% O2 for 15 min). Sixty minutes after the onset of hypoxia induction, pups received either MSC-exosomes (30 µg/100 µL) or saline for 12 consecutive days (lactation period). Behavioral tests, hippocampal tissue analysis (for RT-PCR and oxidative stress markers), and pentylenetetrazole (PTZ) kindling were performed at P60-P61. The study revealed that treatment with exosomes improved memory performance and reduced anxiety-like behaviors in the hypoxia-exposed group, as evidenced by the novel object recognition and elevated plus maze tests. These benefits were linked to decreased oxidative stress (lower malondialdehyde/MDA levels), reduced pro-inflammatory markers (interleukin-6 [IL-6] and tumor necrosis factor-α [TNF-α]), and increased anti-inflammatory signaling (higher IL-10) in the hippocampus. Although exosome therapy delayed the onset of epileptogenesis, it did not lessen the intensity of seizures. The results indicate that administering MSC-derived exosomes after HINS can reduce susceptibility to PTZ-induced kindling, alleviate neuroinflammation, regulate oxidative stress, and protect against long-term cognitive impairments. Together, these findings highlight the potential of exosome-based interventions in mitigating the delayed neurological effects of HINS during adolescence.
    Keywords:  HINS; anxiety; exosome; inflammation; memory; rat
    DOI:  https://doi.org/10.1002/dneu.23010
  9. J Orthop Surg Res. 2025 Oct 21. 20(1): 902
       BACKGROUND: Osteoblast formation and function are essential for regulating bone disorders such as osteoporosis. Recent studies have confirmed that long non-coding RNAs (lncRNAs) from exosomes (ExOs) are involved in osteoblast proliferation and differentiation. This study investigated the role of bone marrow mesenchymal stem cell (BMSC)-derived exosomal lncRNA-ZFAS1 in regulating osteoblasts.
    METHODS: Human BMSCs and derived exosomes (BMSC-EXOs) were isolated and characterized. ZFAS1, miR-9, and IGF-1 levels in BMSC-EXOs and osteoblasts were measured by RT-qPCR and Western blot. ZFAS1 localization was determined by fluorescence in situ hybridization (FISH) and nuclear-cytoplasmic fractionation. ZFAS1 interactions with miR-9 and IGF-1 were confirmed via dual-luciferase reporter assay and RNA-binding protein immunoprecipitation (RIP). The effects of the ZFAS1/miR-9 axis on osteoblast proliferation and differentiation were examined using CCK-8, Alizarin Red staining, and ALP staining assays.
    RESULTS: BMSC-EXOs exhibited elevated ZFAS1 levels and efficiently delivered this lncRNA to osteoblasts. Through this mechanism, ZFAS1 enhanced osteoblast proliferation and differentiation. Mechanistically, ZFAS1 inhibited miR-9 expression, and downregulation of miR-9 reversed the suppression of osteoblast proliferation and differentiation induced by ZFAS1 silencing. The decrease in miR-9 leads to an increase in IGF-1, thereby promoting the proliferation and differentiation of osteoblasts.
    CONCLUSIONS: We have shown that ZFAS1 from BMSC-derived EXOs enhances the proliferation and differentiation of osteoblasts by regulating the miR-9/IGF-1 signaling axis. This discovery provides novel insights into mechanisms of osteoblast proliferation and differentiation, and identifies potential therapeutic targets for treating associated diseases.
    Keywords:  Exosome; IGF-1; LncRNA-ZFAS1; MiR-9; Osteoblasts
    DOI:  https://doi.org/10.1186/s13018-025-06310-0
  10. World J Diabetes. 2025 Oct 15. 16(10): 109815
       BACKGROUND: Glucotoxic pancreatic β cells impair glycogenesis of hepatocytes, with exosomes serving as novel mediators. miR-375-3p is the most abundant miRNA in the pancreas and critical for β-cell function, but whether it plays a role in pancreas-liver crosstalk remains unclear.
    AIM: To investigate the role of miR-375-3p, a key regulator of pancreatic β cells, in remotely regulating hepatocyte glycogenesis via exosomes.
    METHODS: Mice fed a high-fat diet (HFD) served as animal models, and mouse primary pancreatic islet cells and the β-cell line MIN-6 were used as cellular models. miR-375-3p expression in pancreatic cells, hepatocytes and exosomes was detected in both animal and cellular models. Transwell assays, exosome treatment, and exosome-depleted supernatant culture were used to investigate the role of exosomal miR-375-3p in pancreatic-hepatocyte crosstalk. The AKT/GSK signaling pathway and hepatic glycogen content were used as indicators to evaluate hepatocyte glycogenesis. Luciferase reporter assays were used to evaluate the downstream targets of miR-375-3p.
    RESULTS: Increased levels of miR-375-3p were observed in both the pancreas and liver of HFD-fed mice. In contrast to the in vivo results, high-glucose treatment exclusively increased the expression of miR-375-3p in pancreatic cells but had no effect on hepatocytes. Furthermore, hepatocytes treated with the supernatant and exosomes from glucotoxic pancreatic cells presented elevated expression of miR-375-3p. Additionally, exosomal transfer of miR-375-3p from pancreatic cells to hepatocytes suppressed the AKT/GSK signaling pathway, thereby reducing the hepatic glycogen content. Luciferase analysis indicated that the recombination signal binding protein for the immunoglobulin kappa J region (Rbpj) is a target gene of miR-375-3p. Rbpj inhibition impaired hepatic glycogenesis, and Rbpj overexpression reversed the effect on glycogenesis induced by miR-375-3p.
    CONCLUSION: Pancreatic cell-derived miR-375-3p can be delivered to hepatocytes via exosomes and inhibits hepatocyte glycogenesis by targeting Rbpj.
    Keywords:  Exosomes; Glycogenesis; Hepatocytes; Pancreatic β cell; miR-375-3p
    DOI:  https://doi.org/10.4239/wjd.v16.i10.109815