ArticleOxidative medicine and cellular longevity2021
Inhibiting miR-205 Alleviates Cardiac Ischemia/Reperfusion Injury by Regulating Oxidative Stress, Mitochondrial Function, and Apoptosis.
Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06256965 (Left Ventricular Ejection Fraction and Oxidative Stress Markers in Patients Subjected to Car-diac Surgery With Cardiopulmonary Bypass), which is not on this map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Left Ventricular Ejection Fraction and Oxidative Stress Markers in Patients Subjected to Car-diac Surgery With Cardiopulmonary Bypass
Who cites it
14 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
- The Wound-Heart Axis: Can Chronic Wounds Contribute to Cardiac Dysfunction?International journal of molecular sciences · 2026Review
- Rg1-R1 attenuates cardiac ischemia/reperfusion-induced endothelial cell injury through activating the ULK1/PGAM5-FUNDC1-mitophagy pathway.Journal of ginseng research · 2026Article
- Oxidative Stress and NLRP3 Inflammasome as Markers of Cardiac Injury Following Cardiopulmonary Bypass: Potential Implications for Patients with Preoperative Heart Failure with Reduced Ejection Fraction.Antioxidants (Basel, Switzerland) · 2025Article
- Molecular Mechanism of Aerobic Exercise Ameliorating Myocardial Mitochondrial Injury in Mice with Heart Failure.International journal of molecular sciences · 2025Article
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- MicroRNA205: A Key Regulator of Cardiomyocyte Transition from Proliferative to Hypertrophic Growth in the Neonatal Heart.International journal of molecular sciences · 2024Article
- MicroRNAs expression profile in chemotherapy-induced cardiotoxicity in NSCLC using a co-culture model.Biomolecules & biomedicine · 2024Article
- MicroRNA profiling of the feline left heart identifies chamber-specific expression signatures in health and in advanced hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology plus · 2023Article
- Identification of a circulating microRNAs biomarker panel for non-invasive diagnosis of coronary artery disease: case-control study.BMC cardiovascular disorders · 2022Article
- Mitochondrial health quality control: measurements and interpretation in the framework of predictive, preventive, and personalized medicine.The EPMA journal · 2022Review
- Soluble RAGE attenuates myocardial I/R injuries via FoxO3-Bnip3 pathway.Cellular and molecular life sciences : CMLS · 2022Article
- Phosphorylated nuclear factor erythroid 2-related factor 2 promotes the secretion of C-C motif chemokine ligand 2 and the recruitment of M2 macrophages.Annals of translational medicine · 2021Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundmiR-205 is important for oxidative stress, mitochondrial dysfunction, and apoptosis. The roles of miR-205 in cardiac ischemia/reperfusion (I/R) injury remain unknown. The aim of this research is to reveal whether miR-205 could regulate cardiac I/R injury by focusing upon the oxidative stress, mitochondrial function, and apoptosis.
methodsLevels of miR-205 and Rnd3 were examined in the hearts with I/R injury. Myocardial infarct size, cardiac function, oxidative stress, mitochondria function, and cardiomyocyte apoptosis were detected in mice with myocardial ischemia/reperfusion (MI/R) injury. The primary neonatal cardiomyocytes underwent hypoxia/reoxygenation (H/R) to simulate MI/R injury.
resultsmiR-205 levels were significantly elevated in cardiac tissues from I/R in comparison with those from Sham. In comparison with controls, levels of Rnd3 were significantly decreased in the hearts from mice with MI/R injury. Furthermore, inhibiting miR-205 alleviated MI/R-induced apoptosis, reduced infarct size, prevented oxidative stress increase and mitochondrial fragmentation, and improved mitochondrial functional capacity and cardiac function. Consistently, overexpression of miR-205 increased infarct size and promoted apoptosis, oxidative stress, and mitochondrial dysfunction in mice with MI/R injury. In cultured mouse neonatal cardiomyocytes, downregulation of miR-205 reduced oxidative stress in H/R-treated cardiomyocytes. Finally, inhibiting Rnd3 ablated the cardioprotective effects of miR-205 inhibitor in MI/R injury.
conclusionsWe conclude that inhibiting miR-205 reduces infarct size, improves cardiac function, and suppresses oxidative stress, mitochondrial dysfunction, and apoptosis by promoting Rnd3 in MI/R injury. miR-205 inhibitor-induced Rnd3 activation is a valid target to treat MI/R injury.
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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.