bims-evecad 2026-07-12 papers

bims-evecad

Biomed News

on Extracellular vesicles and cardiovascular disease

Issue of 2026–07–12
seven papers selected by
Cliff Dominy

The Role of Extracellular Vesicles in the Pathogenesis of Hypertension.
Bench to Bedside: Insights from Large Animal Models and Emerging Clinical Trials of Endogenous Cardiac Regeneration and Repair.
ANY ROLE FOR RENAL-DERIVED EXTRACELLULAR VESICLES MANIPULATION FOR CARDIOPROTECTION IN CKD?
Plant-derived extracellular vesicles as emerging cardioprotective agents for cardiovascular diseases.
Molecular and imaging biomarkers in myocardial ischemia/reperfusion injury: from pathogenetic mechanisms to therapeutic targeting.
Extracellular Vesicles Mediate Activation and Trafficking of Splenic Immune Cells to the Heart Post-Myocardial Infarction.
Intercellular Mitochondrial Transfer and Mitochondrial Transplantation in Cardiovascular Disease.

Electrolyte Blood Press. 2026 Jun;24(2): 120-128

The Role of Extracellular Vesicles in the Pathogenesis of Hypertension.

Seung Hee Jeong, In O Sun.

  Hypertension is one of the most common health problems and a leading global risk factor for cardiovascular, cerebrovascular, and renal diseases. The pathogenesis of essential hypertension is complex, and many organs, such as the heart, kidneys, arteries, and immune system, are involved in its pathophysiology. Extracellular vesicles (EVs) are membrane-bound nanosized structures that are generated and released into the extracellular fluid by all cell types. They mediate cell-to-cell communication in various physiological and pathophysiological processes. Therefore, EVs may play pivotal roles in the pathogenesis and systemic progression of diverse pathological conditions, including inflammatory, vascular, neoplastic, infectious, and neurodegenerative disorders. Emerging evidence has underscored their involvement in the development and progression of hypertension. Circulating and urinary EVs are promising diagnostic, prognostic, and therapeutic biomarkers of cardiovascular diseases, including hypertension. Moreover, EV-mediated therapies, particularly engineered EVs designed for precise drug delivery, are currently being developed for the treatment of various cardiovascular disorders, including hypertension and myocardial infarction. This review explores the role of EVs in the pathogenesis of hypertension and summarizes their potential as diagnostic and prognostic biomarkers.

Keywords:  Biomarker; Exosomes; Hypertension; Pathology; Physiology

DOI:  https://doi.org/10.5049/EBP.2026.24.e8
J Cardiovasc Transl Res. 2026 Jul 08. pii: 85. [Epub ahead of print]19(1):

Bench to Bedside: Insights from Large Animal Models and Emerging Clinical Trials of Endogenous Cardiac Regeneration and Repair.

Shu-Xuan Chen, Liu-Hua Zhou, Tong-Tong Yang, Hao Wang, Lian-Sheng Wang.

  Cardiovascular disease (CVD), particularly myocardial infarction (MI), remains a leading cause of morbidity and mortality worldwide. The irreversible loss of cardiomyocytes (CMs) and subsequent fibrosis following MI due to delayed or absent reperfusion are central drivers of heart failure progression. Recent evidence indicates that the adult mammalian heart retains a latent regenerative capacity, which can be reactivated under specific conditions. Therefore, stimulating endogenous cardiac regeneration represents a promising strategy to improve clinical outcomes following MI. This review summarizes a range of intervention strategies designed to wake up cardiac regeneration and promote myocardial repair in the setting of residual following myocardial injury. Key approaches examined include stimulating cardiomyocyte cell-cycle re-entry, leveraging growth factors and paracrine mediators as pro-regenerative signals, and applying cell-free vesicles and small molecule compounds. We discuss the translational progress of these strategies, drawing on evidence from large animal models and ongoing clinical trials, aiming to bridge mechanistic discoveries to future clinical applications in cardiac regenerative medicine.

Keywords:  Cardiomyocyte proliferation; Endogenous cardiac regeneration; Intervention strategies; Myocardial infarction

DOI:  https://doi.org/10.1007/s12265-026-10808-1
Nephron. 2026 Jul 08. 1-10

ANY ROLE FOR RENAL-DERIVED EXTRACELLULAR VESICLES MANIPULATION FOR CARDIOPROTECTION IN CKD?

Aneliya Parvanova, Piero Ruggenenti.

DOI: https://doi.org/10.1159/000552762
J Nanobiotechnology. 2026 Jul 06.

Plant-derived extracellular vesicles as emerging cardioprotective agents for cardiovascular diseases.

Qian Li, Zhen Wang, Qianqian Huang, Nanbo Zheng, Bingtao Zhai, Dongyan Guo, Junbo Zou, Yajun Shi, Fei Luan.

  Cardiovascular diseases (CVDs) remain a leading cause of global morbidity and mortality. Their complex and multifactorial pathogenesis, involving endothelial dysfunction, chronic inflammation, oxidative stress, metabolic dysregulation, and pathological remodeling, limits the long-term effectiveness of current therapeutic strategies and underscores the need for novel treatment approaches. Plant-derived extracellular vesicles (PDEVs) have recently emerged as promising cardioprotective agents because of their favorable biocompatibility, relatively low immunogenicity, abundant endogenous bioactive cargoes, and engineering flexibility. Owing to these properties, PDEVs possess dual characteristics as natural nanocarriers and bioactive therapeutic agents. Preclinical evidence from various in vitro and in vivo cardiovascular disease models indicates that PDEVs exert antioxidative, anti-inflammatory, immunomodulatory, and tissue-reparative effects, thereby attenuating myocardial injury, reducing oxidative stress, and promoting cardiomyocyte survival. Beyond their intrinsic therapeutic activities, PDEVs can also serve as multifunctional drug delivery vehicles for small-molecule drugs, nucleic acids, proteins, and natural bioactive compounds, improving cargo stability, bioavailability, and therapeutic performance. Recent advances in surface functionalization, membrane fusion, and biomimetic design have further enhanced their targeting capacity and functional controllability. This review focuses on the application of PDEVs in cardiovascular disease therapy, systematically summarizing their preparation, characterization, quality evaluation, and relative advantages and limitations compared with conventional nanocarriers. It further highlights their therapeutic effects in different cardiovascular disease models, drug delivery applications, engineering strategies, and the current progress and key challenges in clinical translation. Continued advances in this field may promote the translation of PDEVs from experimental research to clinical application and broaden their value in cardiovascular nanomedicine.

Keywords:  Cardiovascular diseases; Clinical research; Drug delivery systems; Membrane engineering; Plant-derived extracellular vesicles

DOI:  https://doi.org/10.1186/s12951-026-04765-9
Expert Rev Cardiovasc Ther. 2026 Jul 10.

Molecular and imaging biomarkers in myocardial ischemia/reperfusion injury: from pathogenetic mechanisms to therapeutic targeting.

Athina Nasoufidou, Marios G Bantidos, Christos Kofos, Nikolaos Stalikas, Andreas Mitsis, Panagiotis Stachteas, Paschalis Karakasis, Maria Fasoula, Barbara Fyntanidou, George Kassimis, Nikolaos Fragakis, Efstratios Karagiannidis.

   INTRODUCTION: Ischemic heart disease remains a leading cause of morbidity and mortality worldwide despite advances in diagnosis, revascularization, and risk-factor control. Myocardial ischemia/reperfusion (I/R) injury (MIRI) is a multiphase process evolving over minutes to weeks, contributing to infarct expansion, microvascular obstruction, intramyocardial hemorrhage, and adverse ventricular remodeling. High-sensitivity cardiac troponins remain central to diagnosing myocardial necrosis but provide limited mechanistic insight into upstream MIRI processes.
AREAS COVERED: For this review, PubMed/MEDLINE and Scopus were searched from inception to May 2026. Established and emerging biomarkers are examined across the I/R continuum, including tissue-derived markers, inflammatory and oxidative-stress mediators, endothelial and neurohormonal biomarkers, remodeling-related proteins, non-coding RNAs, cell-free DNA, extracellular vesicles, metabolomic and proteomic signatures, and multi-omics platforms. Cardiac magnetic resonance and positron emission tomography are also analyzed for tissue characterization and complication detection.
EXPERT OPINION: The most realistic role for MIRI biomarkers is selective post-reperfusion phenotyping, as high-sensitivity cardiac troponins will remain the diagnostic anchor in acute myocardial infarction. Their initial clinical value is likely prognostic, refining risk stratification and follow-up intensity. Translation will require standardized assays, harmonized sampling, evidence of incremental value, and prospective demonstration that biomarker-guided decisions improve outcomes, resource allocation, cost-effectiveness, and trial efficiency.

Keywords:  Cardioprotection; inflammation; ischemic heart disease; multi-omics; oxidative stress; translational research

DOI:  https://doi.org/10.1080/14779072.2026.2703072
bioRxiv. 2026 Jun 29. pii: 2026.06.23.734125. [Epub ahead of print]

Extracellular Vesicles Mediate Activation and Trafficking of Splenic Immune Cells to the Heart Post-Myocardial Infarction.

Kaneez Fatima, Austin Angelotti, Vinay Kumar, Vishnu Chollangi, Wafa Aziz, Siddarth Dasari, Emily N Bianchini, Joseph Wang, Suman Asalla, Harpreet Singh, Sumanth D Prabhu, Shyam S Bansal.

Background: Myocardial infarction (MI) triggers splenic immune cell trafficking to the heart. Vehicles that carry these signals and mediate this crosstalk are unknown.
Hypothesis: We hypothesize that extracellular vesicles (EVs) released post-MI mediate splenic immune trafficking to the heart.
Methods: Mice were treated daily with an EV biogenesis inhibitor (GW4869) or vehicle. Splenic/cardiac immune cells were assessed at 3d while survival, cardiac function, hypertrophy, and fibrosis were evaluated at 8w post-MI. Plasma EVs from 1d MI mice or from the hearts that underwent MI/sham in a Langendorff system induced splenic immune trafficking to the heart within 3d and systolic dysfunction at 8w in naïve mice.
Results: GW4869 i) inhibited splenic regression, ii) increased splenic retention of neutrophils, monocytes, dendritic cells (DCs), and CD4⁺ T-cells, iii) decreased cardiac gene expression of pro-inflammatory cytokines/chemokines, and iv) decreased trafficking of immune cells to the hearts at 3d post-MI, and iii) improved systolic function and attenuated hypertrophy at 8w post-MI. MI EVs accumulated in the spleen and promoted egress of matured splenic immune cells upon administration to naïve mice. Cardiac pro-inflammatory cytokines/chemokines expression and CCR2 + MHC-II hi infiltrating macrophages, CD11c + DCs, and CD4 + and CD4 + TNFα + T-cell levels were also increased in naïve mice at 3d post-injection. Importantly, transfer of MI EVs for 2 days induced systolic dysfunction, cellular hypertrophy, and fibrosis in naïve mice at 8 w post-injection. DCs process MI EVs for T-cells activation.
Conclusions: EVs mobilize splenic immune cells to the heart post-MI and their inhibition can subdue inflammatory tissue-damage to promote healing post-MI.

DOI: https://doi.org/10.64898/2026.06.23.734125
Can J Cardiol. 2026 Jul 07. pii: S0828-282X(26)00654-9. [Epub ahead of print]

Intercellular Mitochondrial Transfer and Mitochondrial Transplantation in Cardiovascular Disease.

Fatemeh Farhid, Farshad Heydari, Michael R Hamblin, Saman Masoudifar, Amirhossein Sahebkar, Jalal Naghinezhad.

  Mitochondria have traditionally been regarded as intracellular powerhouses; however, they are now recognized as dynamic intercellular signaling organelles capable of moving between cells to coordinate tissue adaptation and repair. This Review examines the emergence of mitochondria transfer as a fundamental mechanism of cardiovascular communication, integrating current evidence for the exchange of intact mitochondria, mitochondrial DNA, and mitochondrial components among cardiomyocytes, endothelial cells, vascular smooth muscle cells, fibroblasts, and immune cells. We discuss the major routes of mitochondria transfer, including tunneling nanotubes, extracellular vesicles, gap junction-associated pathways, and extracellular mitochondrial release, together with the molecular machinery governing mitochondrial trafficking, such as MIRO proteins, TRAK adaptors, and cytoskeletal motor complexes. By reshaping cellular bioenergetics, redox homeostasis, metabolic signaling, and innate immune responses, transferred mitochondria exert profound effects on cardiovascular homeostasis and disease, influencing ischemia-reperfusion injury, heart failure, vascular remodeling, and inflammatory vascular disorders. We further evaluate recent advances in mitochondria transplantation, engineered mitochondrial donor platforms, and emerging imaging technologies that enable tracking of mitochondrial fate in vivo. Finally, we propose an integrated mechanistic framework in which the biological consequences of mitochondria transfer and mitochondria transplantation are determined by donor-recipient compatibility, mitochondrial quality, and the surrounding microenvironment, thereby explaining their context-dependent protective, maladaptive, and immunomodulatory effects. By identifying critical gaps in molecular mechanisms, methodological standardization, and clinical validation, this Review outlines a roadmap for translating mitochondria-based therapeutic strategies into precision cardiovascular medicine.

Keywords:  Bioenergetics; Cardiovascular disease; Extracellular vesicles; Heart failure; Mitochondrial transfer; Mitochondrial transplantation; Regenerative cardiology

DOI:  https://doi.org/10.1016/j.cjca.2026.06.032