ArticleCardiovascular research2025
miR-24-3p secreted as extracellular vesicle cargo by cardiomyocytes inhibits fibrosis in human cardiac microtissues.
Article in Cardiovascular research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The Origin and Application of Cardiomyocyte-Derived Small Extracellular Vesicles: A Systematic Review.International journal of medical sciences · 2026Pooled it
- Cardiac fibrosis: mechanistic insights and translational advances.Molecular biomedicine · 2026Review
- Structural and Functional Abnormalities in the Preterm Heart: From Development to Adulthood.Journal of the American Heart Association · 2026Review
- Extracellular vesicles in the heart: mediators of intercellular communication in health and disease in vitro.Cell communication and signaling : CCS · 2026Review
- Vascular endothelial cell-derived small extracellular vesicles: A protective role against cardiomyocyte apoptosis in ischemia-reperfusion injury through miR410-3p-modulatedThe Journal of international medical research · 2026Article
- Integrating network toxicology, machine learning, and molecular dynamics simulations to reveal tanshinone iia's dual mechanisms in TNBC and doxorubicin-induced cardiotoxicity.Scientific reports · 2026Article
- Extracellular Vesicles in the Heart-Organ Axis: From Inter-Organ Communication to Precision Nanomedicine for Heart Diseases.International journal of nanomedicine · 2026Review
- Heterogeneity and Clinical Translation of Cardiac-Derived Extracellular Vesicles in Heart Failure: From Mechanisms to Precision Therapeutics.Reviews in cardiovascular medicine · 2026Review
- RUNX1-mediated repression of miR-24 promotes hepatic stellate cell activation and liver fibrosis by targeting the ALK4/Smad3 signaling pathway.Frontiers in genetics · 2026Article
- Extracellular Vesicles in Cardiovascular Diseases: Signaling, Biomarker, and Therapy.Journal of cardiovascular translational research · 2025Review
- miR-24-3p mediates Keap1/Nrf2 axis to promote autophagy and thereby inhibit lens epithelial cell early senescence.International ophthalmology · 2025Article
- Living myocardial slices: walking the path towards standardization.Cardiovascular research · 2025Review
- Extracellular vesicles in cardiovascular diseases: pathogenic mediators, diagnostic tools, and therapeutic vectors.Frontiers in cardiovascular medicine · 2025Review
- Stem-Cell Derived Exosomal microRNAs as Biomarkers and Therapeutics for Pediatric Cardiovascular Disease.Current treatment options in cardiovascular medicine · 2025Review
- Cryopreservation of Human Adult Ventricular Tissue for the Preparation of Viable Myocardial Slices.Current protocols · 2024Article
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Authors and funding
18 authors.
Funding
Abstract
aimsCardiac fibrosis in response to injury leads to myocardial stiffness and heart failure. At the cellular level, fibrosis is triggered by the conversion of cardiac fibroblasts (CF) into extracellular matrix-producing myofibroblasts. miR-24-3p regulates this process in animal models. Here, we investigated whether miR-24-3p plays similar roles in human models. METHODS AND
resultsGain- and loss-of-function experiments were performed using human induced pluripotent stem cell-derived cardiomyocytes (hCM) and primary hCF under normoxic or ischaemia-simulating conditions. hCM-derived extracellular vesicles (EVs) were added to hCF. Similar experiments were performed using three-dimensional human cardiac microtissues and ex vivo cultured human cardiac slices. hCF transfection with miR-24-3p mimic prevented TGFβ1-mediated induction of FURIN, CCND1, and SMAD4-miR-24-3p target genes participating in TGFβ1-dependent fibrogenesis-regulating hCF-to-myofibroblast conversion. hCM secreted miR-24-3p as EV cargo. hCM-derived EVs modulated hCF activation. Ischaemia-simulating conditions induced miR-24-3p depletion in hCM-EVs and microtissues. Similarly, hypoxia down-regulated miR-24-3p in cardiac slices. Analyses of clinical samples revealed decreased miR-24-3p levels in circulating EVs in patients with acute myocardial infarction (AMI), compared with healthy subjects. Post-mortem RNAScope analysis showed miR-24-3p down-regulation in myocardium from patients with AMI, compared with patients who died from non-cardiac diseases. Berberine, a plant-derived agent with miR-24-3p-stimulatory activity, increased miR-24-3p contents in hCM-EVs, down-regulated FURIN, CCND1, and SMAD4, and inhibited fibrosis in cardiac microtissues.
conclusionThese findings suggest that hCM may control hCF activation through miR-24-3p secreted as EV cargo. Ischaemia impairs this mechanism, favouring fibrosis.
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