ArticleAmerican journal of translational research2025
Endothelial progenitor cell-derived microvesicles therapy relieves myocardial infarction symptoms by altering left ventricular protein expression.
Article in American journal of translational research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- The Role and Mechanism of Endothelial Progenitor Cell-Derived Extracellular Vesicles in Vascular Repair of Ischemic Heart Disease.Journal of cardiovascular translational research · 2026Review
- Application and Future Perspectives of Extracellular Vesicle-Loaded Scaffold in Spinal Cord Injury.International journal of nanomedicine · 2026Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the therapeutic potential of endothelial progenitor cell-derived microvesicles (EPC-MVs) in a rat myocardial infarction (MI) model, focusing on their effects on inflammation, apoptosis, and global proteomic changes in the left ventricle.
methodsEndothelial progenitor cells (EPCs) were isolated from mouse bone marrow, and microvesicles (MVs) were derived and injected into rats with MI induced by ligation of the left anterior descending artery. Therapeutic efficacy was assessed by measuring inflammatory cytokines (TNF-α, IL-6) and cardiac injury markers (creatine kinase-MB, myoglobin), along with histologic and apoptotic analyses. A global proteomic analysis of left ventricular tissue was performed to explore the underlying molecular mechanisms. Key targets, including components of the NLRP3 inflammasome (NLRP3, Caspase-1, apoptosis-associated speck-like protein containing a CARD), were validated by western blotting.
resultsEPC-MV treatment significantly reduced MI-induced cardiac injury, as evidenced by decreased inflammatory cytokines and cardiac injury markers, preservation of myocardial architecture, reduced fibrosis, and suppression of cardiomyocyte apoptosis. Proteomic analysis revealed significant alterations in inflammatory and metabolic pathways, supported by KEGG and Reactome enrichment analyses. Molecular validation confirmed that EPC-MVs inhibited the activation of the NLRP3 inflammasome and downregulated downstream effectors, including IL-6 and atrial natriuretic peptide.
conclusionEPC-MVs alleviated myocardial ischemic injury by remodeling the cardiac proteome, suppressing inflammatory and apoptotic signaling. These results position EPC-MVs as a promising cell-free therapeutic strategy for MI.
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