ArticleExperimental and therapeutic medicine2019
MicroRNA-138 attenuates myocardial ischemia reperfusion injury through inhibiting mitochondria-mediated apoptosis by targeting HIF1-α.
Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 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
- The Role of miR-138 in Cardiovascular Diseases.BioMed research international · 2025Review
- Hypoxic Inducible Factor Stabilization in Pericytes beyond Erythropoietin Production: The Good and the Bad.Antioxidants (Basel, Switzerland) · 2024Review
- MicroRNA-214-3p protects against myocardial ischemia-reperfusion injury by targeting demethylase lysine demethylase 3A.Regenerative therapy · 2023Article
- Comprehensive Analysis of Mitochondrial Dynamics Alterations in Heart Diseases.International journal of molecular sciences · 2023Review
- Mechanisms shared between cancer, heart failure, and targeted anti-cancer therapies.Cardiovascular research · 2023Review
- The Role of Angiogenesis and Arteriogenesis in Myocardial Infarction and Coronary Revascularization.Journal of cardiovascular translational research · 2022Review
- MicroRNA-124a Protects the Myocardium Against Ischemia Reperfusion Injury Through Regulation of the Notch Signaling Pathway.Brazilian journal of cardiovascular surgery · 2022Article
- Leveraging Extracellular Non-coding RNAs to Diagnose and Treat Heart Diseases.Journal of cardiovascular translational research · 2022Review
- MiR-494-3p Upregulation Exacerbates Cerebral Ischemia Injury by Targeting Bhlhe40.Yonsei medical journal · 2022Article
- LncRNA LINC00461 exacerbates myocardial ischemia-reperfusion injury via microRNA-185-3p/Myd88.Molecular medicine (Cambridge, Mass.) · 2022Article
- Perspectives on mitochondrial relevance in cardiac ischemia/reperfusion injury.Frontiers in cell and developmental biology · 2022Review
- Cardioprotective Effect of circ_SMG6 Knockdown against Myocardial Ischemia/Reperfusion Injury Correlates with miR-138-5p-Mediated EGR1/TLR4/TRIF Inactivation.Oxidative medicine and cellular longevity · 2022Article
- Overexpression of miR-1298 attenuates myocardial ischemia-reperfusion injury by targeting PP2A.Journal of thrombosis and thrombolysis · 2022Article
- Review
- Advances in the mechanism and treatment of mitochondrial quality control involved in myocardial infarction.Journal of cellular and molecular medicine · 2021Review
- HIF‑1α in myocardial ischemia‑reperfusion injury (Review).Molecular medicine reports · 2021Review
- Involvement of non‑coding RNAs in the pathogenesis of myocardial ischemia/reperfusion injury (Review).International journal of molecular medicine · 2021Review
- Hyperoside protects cardiomyocytes against hypoxia‑induced injury via upregulation of microRNA‑138.Molecular medicine reports · 2021Article
- Up-regulating microRNA-138-5p enhances the protective role of dexmedetomidine on myocardial ischemia-reperfusion injury mice via down-regulating Ltb4r1.Cell cycle (Georgetown, Tex.) · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial ischemia-reperfusion (I/R) injury is considered to have a detrimental role in coronary heart disease, which is considered to be the leading cause of death worldwide. However, the molecular mechanism involved in the progression of myocardial I/R injury is still unclear. The current study aimed to investigate the expression and function of microRNA (miR)-138 in the process of myocardial I/R injury. First, miR-138 expression levels were analyzed both in myocardium with I/R injury and control myocardium using reverse transcription-quantitative polymerase chain reaction analysis. Then, the relationship between the levels of miR-138 and hypoxia-inducible factor (HIF)1-α was also investigated using a luciferase reporter assay. Assessment of myocardial infarct size, measurements of serum myocardial enzymes and electron microscopy analysis were all utilized to analyse the effect of miR-138 on myocardial I/R injury. The authors of current study also used western blotting to examine the expression levels of the mitochondrial fission-related proteins dynamin-1-like protein and mitochondrial fission 1 protein. It was found that miR-138 is downregulated and HIF1-α is upregulated after myocardial ischemia reperfusion injury. Overexpression of miR-138 reduced myocardial I/R injury-induced infarct sizes and myocardial enzyme levels, and it also inhibited the expression of proteins related to mitochondrial morphology and myocardial I/R-induced mitochondrial apoptosis by targeting HIF1-α. Taken together, these findings provide a novel insight into the molecular mechanism of miR-138 and HIF1-α in the progression of myocardial I/R injury. miR-138 has the potential to become a promising therapeutic target for treating myocardial I/R injury.
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Registered trials
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