ArticleJournal of thrombosis and thrombolysis2021
MicroRNA-520d-3p alleviates hypoxia/reoxygenation-induced damage in human cardiomyocytes by targeting ATG-12.
Article in Journal of thrombosis and thrombolysis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- miR‑18a‑5p Serves as a Diagnostic and Prognostic Biomarker and Attenuates Hypoxia‑Induced Cardiac Microvascular Endothelial Injury by Targeting the HIF1A/NF‑κB Pathway in Chronic Heart Failure.Cardiovascular drugs and therapy · 2026Article
- Myocardium miRNA Analysis Reveals Potential Biomarkers of Sudden Coronary Death in Rats.Current issues in molecular biology · 2025Article
- Cardiovascular diseases in the elderly: possibilities for modulating autophagy using non-coding RNAs.Frontiers in cell and developmental biology · 2025Review
- Crosstalk between myocardial autophagy and sterile inflammation in the development of heart failure.Autophagy reports · 2024Review
- The Effects of MicroRNAs in the Development of Heart Failure.Current cardiology reports · 2023Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypoxia/reoxygenation (H/R) induced injury results in extensive damages to myocardial tissue in patients with coronary heart disease, which leads to heart failure. MicroRNA (miRNA) is thought to be associated with myocardial H/R injury. The purpose of this study was to investigate the in vitro role of microRNA-520d-3p in human myocardial cell (HCM) myocardial H/R injury. MTT method and Annexin V-FITC flow cytometry were employed to measure the viability and apoptosis of H/R treated HCM. RT-qPCR was employed to determine miRNA and mRNA expression. MicroRNA-520d-3p mimic and microRNA-520d-3p inhibitor were used to overexpression and inhibit the expression of microRNA-520d-3p. In addition, pcDNA3.1-ATG12 was used to upregulate ATG12 expression. The protein levels of ATG12, Bcl-2 and autophagy related-genes were determined by western blotting. Hypoxia/reoxygenation (H/R) injury could inhibit cell viability, apoptosis and inhibited microRNA-520d-3p expression in HCM. The down-regulation of microRNA-520d-3p inhibited cell viability and induced apoptosis in HCM. The overexpression of microRNA-520d-3p attenuated the effects of H/R treatment on the viability and apoptosis of HCM cells. In addition, microRNA-520d-3p inhibited the expression of autophagy-associated 12 (ATG12). More importantly, H/R treatment could promote autophagy in HCM, and microRNA-520d-3p mimic transfection could significantly reverse this effect. Our result indicated that overexpression of microRNA-520d-3p attenuated the effect of H/R treatments on cell viability, apoptosis and autophagy, through partly regulating ATG12 expression in HCM.
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