ArticleESC heart failure2020
Cardiomyocyte-derived exosomal microRNA-92a mediates post-ischemic myofibroblast activation both in vitro and ex vivo.
Article in ESC heart failure, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 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
77 citing papers in PubMed, 87 citations in OpenAlex.
- Extracellular Vesicles in Cardiovascular Disease: Intercellular Signaling, Liquid Biopsy Biomarkers, and Therapeutic Translation.Circulation research · 2026Review
- Engineering extracellular vesicles for targeted therapeutic delivery in the heart.Bioscience reports · 2026Review
- GATA4-overexpressing BMSCs-derived exosome regulation of myocardial infarction in mice by key miRNA and apoptosis gene CLU.European journal of medical research · 2026Article
- Dynamics and biodistribution of cardiomyocyte-derived small extracellular vesicles following myocardial infarction: sex differences.American journal of physiology. Heart and circulatory physiology · 2026Article
- Extracellular Vesicles in Cardiovascular Diseases: Signaling, Biomarker, and Therapy.Journal of cardiovascular translational research · 2025Review
- The impact of natural and engineered extracellular vesicles on post-myocardial infarction angiogenesis.Stem cell research & therapy · 2025Review
- Organ-Specific Extracellular Vesicles in the Treatment of Ischemic Acute Organ Injury: Mechanisms, Successes, and Prospects.International journal of molecular sciences · 2025Review
- Enhancing cardiac regeneration: direct reprogramming of fibroblasts into myocardial-like cells using extracellular vesicles secreted by cardiomyocytes.Molecular and cellular biochemistry · 2025Article
- Cardiac endothelial cells and cardiomyocytes alter their communication properties in diabetic mice.Biological research · 2025Article
- The selective sorting of microRNA-4432 into endothelial extracellular vesicles is controlled by a specific RNA binding protein: new insights into the pathophysiology of venous malformations.The British journal of dermatology · 2025Article
- N-terminal domain of CTRP9 promotes cardiac fibroblast activation in myocardial infarction via Rap1/Mek/Erk pathway.Journal of translational medicine · 2025Article
- Inflammatory Cell-Targeted Delivery Systems for Myocardial Infarction Treatment.Bioengineering (Basel, Switzerland) · 2025Review
- Unlocking the Potential of Extracellular Vesicles in Cardiovascular Disease.Journal of cellular and molecular medicine · 2025Review
- Differential expressions of exosomal miRNAs in patients with chronic heart failure and hyperuricemia: diagnostic values of miR-27a-5p and miR-139-3p.Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Article
- The Role of Exosomes in Myocardial Ischemia-Reperfusion Injury.Cardiology · 2025Review
- Elucidating the preventive and therapeutic effects of cardiac telocytes paracrine microRNAs on ischemic heart disease.Frontiers in cardiovascular medicine · 2025Article
- L-Arginine supplementation as mitochondrial therapy in diabetic cardiomyopathy.Cardiovascular diabetology · 2024Article
- Plasma exosomes from patients with coronary artery disease promote atherosclerosis via impairing vascular endothelial junctions.Scientific reports · 2024Article
- Emerging role of sphingolipids and extracellular vesicles in development and therapeutics of cardiovascular diseases.International journal of cardiology. Heart & vasculature · 2024Review
17 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
aimsWe hypothesize that specific microRNAs (miRNAs) within cardiomyocyte-derived exosomes play a pivotal role in the phenoconversion of cardiac myofibroblasts following myocardial infarction (MI). METHODS AND
resultsWe used an established murine model of MI, obtained in vivo via ligation of the left anterior descending coronary artery. We isolated adult cardiomyocytes and fibroblasts, and we assessed the functional role of cardiomyocyte-derived exosomes and their molecular cargo in the activation of cardiac fibroblasts. We identified and biologically validated miR-92a as a transcriptional regulator of mothers against DPP homologues 7 (SMAD7), a known inhibitor of α-smooth muscle actin (α-SMA), established marker of myofibroblast activation. We found that miR-92a was significantly (P < 0.05) upregulated in cardiomyocyte-derived exosomes and in fibroblasts isolated after MI compared with SHAM conditions (n ≥ 6/group). We tested the activation of myofibroblasts by measuring the expression levels of αSMA, periostin, and collagen. Primary isolated cardiac fibroblasts were activated both when incubated with cardiomyocyte-derived exosomes isolated from ischemic cardiomyocytes and when cultured in conditioned medium of post-MI cardiomyocytes, whereas no significant difference was observed following incubation with exosomes or medium from sham cardiomyocytes. These effects were attenuated when an inhibitor of exosome secretion, GW4869 (10 μM for 12 h) was included in the experimental setting. Through means of specific miR-92a mimic and miR-92a inhibitor, we also verified the mechanistic contribution of miR-92a to the activation of cardiac fibroblasts.
conclusionsOur results indicate for the first time that miR-92a is transferred to fibroblasts in form of exosomal cargo and is critical for cardiac myofibroblast activation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.