ArticleClinical and translational medicine2022
Extracellular vesicle-packaged mitochondrial disturbing miRNA exacerbates cardiac injury during acute myocardial infarction.
Article in Clinical and translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 29 citations in OpenAlex.
- ALY688 Protects Against Myocardial Ischemia-Reperfusion Injury via Direct Effects and Rab8a-Dependent Extracellular Vesicles.Journal of extracellular vesicles · 2026Article
- Extracellular Vesicles in Cardiovascular Disease: Intercellular Signaling, Liquid Biopsy Biomarkers, and Therapeutic Translation.Circulation research · 2026Review
- [Targeted inhibition of miR-503 upregulates Apelin expression to alleviate myocardial infarction in mice].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- mBiomolecules · 2026Review
- The Role of NMedComm · 2026Review
- mRedox biology · 2026Review
- RNA modification-mediated multidimensional crosstalk: a novel perspective on gene expression regulation.Genome biology · 2026Review
- Nanoscale Delivery of MicroRNAs via Extracellular Vesicles: Mechanisms Potential in Modulating Cellular Senescence.International journal of nanomedicine · 2026Review
- m6A modification on ncRNAs and underlying mechanisms of exercise in the regulation of pathological cardiac remodeling.European journal of medical research · 2025Review
- Mitochondria-Enriched Extracellular Vesicles (EVs) for Cardiac Bioenergetics Restoration: A Scoping Review of Preclinical Mechanisms and Source-Specific Strategies.International journal of molecular sciences · 2025Article
- The methyltransferase-like proteins as core regulators of nucleic acid modifications and post-translation modification of proteins in disease pathogenesis and therapeutic implications.Biomarker research · 2025Review
- Harnessing miRNA therapeutics: a novel approach to combat heart and brain infarctions in atherosclerosis.Cell death discovery · 2025Review
- METTL3: a multifunctional regulator in diseases.Molecular and cellular biochemistry · 2025Review
- A comprehensive review of m6 A methylation in coronary heart disease.Journal of molecular medicine (Berlin, Germany) · 2025Review
- METTL3-mediated m⁶A methylation in cardiac diseases: pathogenic roles and therapeutic potential.Cell biology and toxicology · 2025Review
- Recent advances in the roles of extracellular vesicles in cardiovascular diseases: pathophysiological mechanisms, biomarkers, and cell-free therapeutic strategy.Molecular medicine (Cambridge, Mass.) · 2025Review
- Enhancing cardiac repair post-myocardial infarction: a study on GATM/Gel hydrogel therapeutics.Cell biology and toxicology · 2025Article
- Review
- NAging and disease · 2024Review
- m6A epitranscriptomic and epigenetic crosstalk in cardiac fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Review
Corrections and comments
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Authors and funding
20 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mounting evidence suggests that extracellular vesicles (EVs) are effective communicators in biological signalling in cardiac physiology and pathology. However, the role of EVs in cardiac injury, particularly in ischemic myocardial scenarios, has not been fully elucidated. Here, we report that acute myocardial infarction (AMI)-induced EVs can impair cardiomyocyte survival and exacerbate cardiac injury. EV-encapsulated miR-503, which is enriched during the early phase of AMI, is a critical molecule that mediates myocardial injury. Functional studies revealed that miR-503 promoted cardiomyocyte death by directly binding to peroxisome proliferator-activated receptor gamma coactivator-1β (PGC-1β) and a mitochondrial deacetylase, sirtuin 3 (SIRT3), thereby triggering mitochondrial metabolic dysfunction and cardiomyocyte death. Mechanistically, we identified endothelial cells as the primary source of miR-503 in EVs after AMI. Hypoxia induced rapid H3K4 methylation of the promoter of the methyltransferase-like 3 gene (METTL3) and resulted in its overexpression. METTL3 overexpression evokes N6-methyladenosine (m
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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.