ArticleInternational journal of biological sciences2019
miR-30e-5p Mitigates Hypoxia-Induced Apoptosis in Human Stem Cell-Derived Cardiomyocytes by Suppressing Bim.
Article in International journal of biological sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- The diagnostic value of miR-338-3p in acute coronary syndrome and its correlation with MACE occurrence.Journal of cardiothoracic surgery · 2026Article
- The MicroRNAs-STAT3-cyclophilin D-cell apoptosis axis: a novel pathway for phosphocreatine treatment in heart disease.Journal of molecular histology · 2026Review
- Unraveling the mechanism of curcumin in coronary slow flow phenomenon through network pharmacology and molecular docking.Scientific reports · 2025Article
- CircFAT1(e2) acts as a sponge for miR-30e-5p and inhibits glioma progression by regulating MYBL2-mediated cell proliferation.Discover oncology · 2025Article
- HMGB1 regulates autophagy via TLR4/NF-κB signaling pathway in myocardial injury induced by coronary microembolization.European journal of medical research · 2025Article
- Advances in Pathophysiology and Novel Therapeutic Strategies for Coronary No-Reflow Phenomenon.Biomedicines · 2025Review
- Mechanistic insight into the role of cardiac-enriched microRNAs in diabetic heart injury.American journal of physiology. Heart and circulatory physiology · 2025Review
- Research Progress of Regulatory Cell Death in Coronary Microembolization.International journal of medical sciences · 2025Review
- Prediction of Early- and Late-Onset Pre-Eclampsia in the Preclinical Stage via Placenta-Specific Extracellular miRNA Profiling.International journal of molecular sciences · 2023Article
- Early growth response-1: Key mediators of cell death and novel targets for cardiovascular disease therapy.Frontiers in cardiovascular medicine · 2023Review
- MicroRNAs in hypertrophic cardiomyopathy: pathogenesis, diagnosis, treatment potential and roles as clinical biomarkers.Heart failure reviews · 2022Review
- miR-30e-5p attenuates neuronal deficit and inflammation of rats with intracerebral hemorrhage by regulating TLR4.Experimental and therapeutic medicine · 2022Article
- miR-30e-5p Alleviates Inflammation and Cardiac Dysfunction After Myocardial Infarction Through Targeting PTEN.Inflammation · 2021Article
- Human Induced Pluripotent Stem Cells as a Disease Model System for Heart Failure.Current heart failure reports · 2021Review
- Melatonin Alleviates LPS-Induced Pyroptotic Cell Death in Human Stem Cell-Derived Cardiomyocytes by Activating Autophagy.Stem cells international · 2021Article
- MicroRNA-Related Strategies to Improve Cardiac Function in Heart Failure.Frontiers in cardiovascular medicine · 2021Review
- miR-30e-5p represses angiogenesis and metastasis by directly targeting AEG-1 in squamous cell carcinoma of the head and neck.Cancer science · 2020Article
- Identification of MicroRNA-Potassium Channel Messenger RNA Interactions in the Brain of Rats With Post-traumatic Epilepsy.Frontiers in molecular neuroscience · 2020Article
- miR-30e-3p Promotes Cardiomyocyte Autophagy and Inhibits Apoptosis via Regulating Egr-1 during Ischemia/Hypoxia.BioMed research international · 2020Article
- Beyond Family: Modeling Non-hereditary Heart Diseases With Human Pluripotent Stem Cell-Derived Cardiomyocytes.Frontiers in physiology · 2020Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coronary microembolization can cause slow or no reflow, which is one of the crucial reasons for reverse of clinical advantage from cardiac reperfusion therapy. miRNAs and apoptosis are dramatically involved in the occurrence and process of cardiovascular diseases. Fortunately, human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) have emerged as an appealing model for the evaluation of cardiovascular diseases. Therefore, our study was designed to explore the role of miR-30e-5p and apoptosis in a hypoxia-induced hiPSC-CM injury model. Our results showed that the expression levels of miR-30e-5p were overtly downregulated in a time-dependent manner under hypoxic conditions. Expression of miR-30e-5p was significantly downregulated after 24 hours of hypoxia, hypoxia treatment dramatically induced apoptosis. Calcium handling capability significantly decreased after 24 hours of hypoxia treatment. miR-30e-5p overexpression partially mitigated hypoxia-induced apoptosis and rescued hypoxia-induced calcium handling defects in hiPSC-CMs. The luciferase reporter assay showed that miR-30e-5p can directly target the 3'-UTR of Bim, which is an apoptosis activator and autophagy suppressor. The mRNA and protein of Bim remarkably increased after hypoxia treatment and reduced with miR-30e-5p overexpression. Moreover, downregulation of Bim mitigated hypoxia-induced apoptosis and activated autophagy. These results demonstrated that miR-30e-5p mitigated hypoxia-induced apoptosis in hiPSC-CMs at least in part via Bim suppression and subsequent autophagy activation. Our study suggested miR-30e-5p may act as a potential therapeutic target for coronary microembolization.
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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.