ArticleBMC cardiovascular disorders2023
The mechanism by which miR-494-3p regulates PGC1-α-mediated inhibition of mitophagy in cardiomyocytes and alleviation of myocardial ischemia-reperfusion injury.
Article in BMC cardiovascular disorders, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Noncoding RNA as potential therapeutics to rescue mitochondrial dysfunction in cardiovascular diseases.American journal of physiology. Heart and circulatory physiology · 2025Pooled it
- Mitophagy in cardiovascular diseases: a literature review.Cardiovascular diagnosis and therapy · 2026Review
- Mitochondrial miRNA- miR-181c-5p and mitomiR-106a-5p levels as indicators in cardiovascular disease patients.Molecular biology reports · 2026Article
- Mastering cardiomyocyte mitophagy: molecular governance, pathological derailment and therapeutics.PeerJ · 2026Review
- Trans-Fatty Acids (TFA) Induced Vascular Injury Through the Regulation of the Sirt1-Ppargc1a-Nfe2l2 Signaling Pathway in Male Rats.Food science & nutrition · 2025Article
- Article
- Effects of acupuncture and moxibustion therapy on endometrial receptivity of infertile women withFrontiers in medicine · 2025Review
- Mitophagy in ischemic heart disease: molecular mechanisms and clinical management.Cell death & disease · 2024Review
- The Impact of the High-Fructose Corn Syrup on Cardiac Damage via SIRT1/PGC1-α Pathway: Potential Ameliorative Effect of Selenium.Biological trace element research · 2024Article
- Unraveling the Etiology of Dilated Cardiomyopathy through Differential miRNA-mRNA Interactome.Biomolecules · 2024Article
- The role of mitophagy in metabolic diseases and its exercise intervention.Frontiers in physiology · 2024Review
- MiR-483-5p downregulation alleviates ox-LDL induced endothelial cell injury in atherosclerosis.BMC cardiovascular disorders · 2023Article
- Unravelling the Interplay between Cardiac Metabolism and Heart Regeneration.International journal of molecular sciences · 2023Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe purpose of this study was to explore whether miR-494-3p inhibits the occurrence of mitochondrial autophagy in cardiomyocytes by inhibiting the expression of PGC1-α and to supplement the theoretical basis for the role of autophagy in cardiac injury induced by hypoxia/reperfusion (H/R).
methodsThe expression of miR-494-3p was detected by RT‒qPCR, and the expression of PGC1-α, autophagy-related proteins (LC3, Beclin 1), apoptosis-related proteins (Bax and Bcl-2), PINK1/Parkin signaling pathway-related proteins (PINK1, Parkin) and mitochondrial change-related proteins (Mfn1, Mfn2, OPA1) was detected by Western blotting. The changes in mitochondrial membrane potential were detected by JC-1 staining (ΔΨm). The formation of autophagosomes was observed by transmission electron microscopy. Cell proliferation activity was detected by CCK-8, and cell apoptosis was detected by flow cytometry. A dual-luciferase gene reporter assay identified a targeted binding site between miR-494-3p and PGC1-α.
resultsThe results showed that miR-494-3p and PGC1-α were differentially expressed in H/R cardiomyocytes; that is, the expression of miR-494-3p was downregulated, and the expression of PGC1-α was upregulated. In addition, mitochondrial autophagy occurred in H/R cardiomyocytes. That is, LC3-II/LC3-I, Beclin 1, PINK1, and Parkin expression was upregulated, Mfn1, Mfn2, and OPA1 expression was downregulated, and the mitochondrial membrane potential was decreased. The transfection of miR-494-3p mimic can significantly improve the cell proliferation activity of cardiomyocytes and inhibit the occurrence of cardiomyocyte apoptosis and autophagy, while the transfection of miR-494-3p inhibitor has the opposite result. After transfection of the miR-494-3p mimic, treatment with autophagy inhibitors and activators changed the effects of miR-494-3p on cardiomyocyte proliferation and apoptosis. At the same time, the overexpression of PGC1-α reversed the promoting effect of miR-494-3p on cardiomyocyte proliferation and the inhibitory effect on apoptosis and autophagy.
conclusionMiR-494-3p can target and negatively regulate the expression of PGC1-α to inhibit mitophagy in cardiomyocytes.
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