ArticleCell death & disease2019
Mitochondrial miR-762 regulates apoptosis and myocardial infarction by impairing ND2.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 97 citations in OpenAlex.
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- The MicroRNAs-STAT3-cyclophilin D-cell apoptosis axis: a novel pathway for phosphocreatine treatment in heart disease.Journal of molecular histology · 2026Review
- The Role of MicroRNAs in Mitochondrial Homeostasis and their Involvement in the Pathogenesis of Obesity and Metabolic Syndrome: A Focus on MicroRNAs.Current medicinal chemistry · 2026Review
- Crosstalk between miRNAs and oxidative stress: implications for cancer pathogenesis and therapy.Functional & integrative genomics · 2025Review
- RNA Therapeutics in Heart Failure.Journal of cardiovascular translational research · 2025Review
- Reductive stress: The key pathway in metabolic disorders induced by overnutrition.Journal of advanced research · 2025Review
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- Mitochondrial Quality Control in Health and Disease.MedComm · 2025Review
- Induction of mitochondrial damage via the CREB3L1/miR-34c/COX1 axis by porcine epidemic diarrhea virus infection facilitates pathogenicity.Journal of virology · 2025Article
- Mitochondrial complex-1 as a therapeutic target for cardiac diseases.Molecular and cellular biochemistry · 2025Review
- Mitochondrial microRNAs (mitomiRs) as emerging biomarkers and therapeutic targets for chronic human diseases.Frontiers in genetics · 2025Review
- Bibliometric Analysis of microRNA: A Comprehensive Evaluation of Its Contribution to Acute Coronary Syndromes.Journal of multidisciplinary healthcare · 2025Review
- White Tea Aqueous Extract: A Potential Anti-Aging Agent Against High-Fat Diet-Induced Senescence inFoods (Basel, Switzerland) · 2024Article
- Exosomal Preconditioning of Human iPSC-Derived Cardiomyocytes Beneficially Alters Cardiac Electrophysiology and Micro RNA Expression.International journal of molecular sciences · 2024Article
- Mitochondrial microRNAs: New Emerging Players in Vascular Senescence and Atherosclerotic Cardiovascular Disease.International journal of molecular sciences · 2024Review
- The miRNA-target interactions: An underestimated intricacy.Nucleic acids research · 2024Review
- Acute endoplasmic reticulum stress-induced mitochondria respiratory chain damage: The role of activated calpains.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Exploring the therapeutic mechanisms of heart failure with Chinese herbal medicine: a focus on miRNA-mediated regulation.Frontiers in pharmacology · 2024Review
- Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction plays a major role in the pathogenesis of cardiovascular diseases. MicroRNAs (miRNAs) are small RNAs that act as negative regulators of gene expression, but how miRNAs affect mitochondrial function in the heart is unclear. Using a miRNA microarray assay, we found that miR-762 predominantly translocated in the mitochondria and was significantly upregulated upon anoxia/reoxygenation (A/R) treatment. Knockdown of endogenous miR-762 significantly attenuated the decrease in intracellular ATP levels, the increase in ROS levels, the decrease in mitochondrial complex I enzyme activity and the increase in apoptotic cell death in cardiomyocytes, which was induced by A/R treatment. In addition, knockdown of miR-762 ameliorated myocardial ischemia/reperfusion (I/R) injury in mice. Mechanistically, we showed that enforced expression of miR-762 dramatically decreased the protein levels of endogenous NADH dehydrogenase subunit 2 (ND2) but had no effect on the transcript levels of ND2. The luciferase reporter assay showed that miR-762 bound to the coding sequence of ND2. In addition, knockdown of endogenous ND2 significantly decreased intracellular ATP levels, increased ROS levels, reduced mitochondrial complex I enzyme activity and increased apoptotic cell death in cardiomyocytes, which was induced by A/R treatment. Furthermore, we found that the inhibitory effect of miR-762 downregulation was attenuated by ND2 knockdown. Thus, our findings suggest that miR-762 participates in the regulation of mitochondrial function and cardiomyocyte apoptosis by ND2, a core assembly subunit of mitochondrial complex I. Our results revealed that mitochondrial miR-762, as a new player in mitochondrial dysfunction, may provide a new therapeutic target for myocardial infarction.
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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.