ArticleAmerican journal of translational research2024
Exosomal miRNA-let-7i-5p from bone marrow mesenchymal stem cells protects against myocardial infarction by inhibiting myocardial apoptosis.
Article in American journal of translational research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Exosomes Enhance Diagnosis and Therapy of Ischemic Heart Disease: Insights and Advances.Journal of cardiovascular translational research · 2026Review
- Circulating exosomal miRNA in acute coronary syndrome: mechanisms, clinical relevance and future directions.Frontiers in molecular biosciences · 2026Review
- Unpacking Exosomes: A Therapeutic Frontier for Cardiac Repair.Current cardiology reports · 2025Review
- Stem-Cell Derived Exosomal microRNAs as Biomarkers and Therapeutics for Pediatric Cardiovascular Disease.Current treatment options in cardiovascular medicine · 2025Review
- microRNAs shuttled by mesenchymal stromal cell-derived exosomes in coronary artery disease: A systematic review of preclinical studies.BioImpacts : BI · 2025Review
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesTo elucidate the regulatory effect of exosomes secreted by bone marrow mesenchymal stem cells (BMSCs-exosomes) on cardiomyocyte apoptosis through miRNA-let-7i-5p in myocardial infarction.
methodsBMSCs-exosomes were extracted, and their morphology and size distribution were analyzed using transmission electron microscope. Expression of exosome surface markers was determined by western blot. H9C2 cells were randomly assigned into five groups, namely control, OGD, OGD+exos, OGD+exos+miR-let-7i-5p inhibitor and OGD+exos+miR-let-7i-5p inhibitor NC. Hypoxic cardiomyocytes were induced using glucose-free Dulbecco's Modified Eagle Medium (DMEM). Mice were randomly assigned into sham, myocardial infarction (MI), MI+exos, MI+exos+miR-let-7i-5p inhibitor and MI+exos+miR-let-7i-5p inhibitor NC groups. MI model was established by ligation of the left anterior descending (LAD) coronary artery. Subsequently, BMSCs-exosomes or BMSCs-exosomes transfected with miRNA-let-7i-5p inhibitor were incubated with hypoxia cardiomyocytes or injected into the MI mouse model. Cell survival was accessed by CCK-8 assay. Cardiomyocyte apoptosis was accessed with V-FITC/PI and TUNEL. Heart function of MI mice was evaluated by echocardiography. Myocardial infarct size was calculated through TTC staining. Relative miRNA-let-7i-5p expression level was determined by RT-qPCR. Expression of apoptosis-related proteins in myocardial tissue were detected by western blot.
resultsExosomes secreted from BMSCs were successfully extracted. In H9C2 cells, miRNA-let-7i-5p expression was significantly upregulated, cell survival rate was increased, and the apoptosis rate was decreased after incubation with BMSCs-exosomes. In MI mice, injection of BMSCs-exosomes markedly upregulated miRNA-let-7i-5p level, reduced infarct size, improved cardiac function, and decreased apoptotic rate. BMSCs-exosomes treatment downregulated Bax and upregulated Bcl-2 protein expression. These effects were reversed by transfection with the miRNA-let-7i-5p inhibitor.
conclusionsBMSCs-exosomes inhibit myocardial apoptosis, attenuate MI progression, and protect against myocardial infarction both
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