ArticleThe Kaohsiung journal of medical sciences2022
MiR-199a-5p promotes ferroptosis-induced cardiomyocyte death responding to oxygen-glucose deprivation/reperfusion injury via inhibiting Akt/eNOS signaling pathway.
Article in The Kaohsiung journal of medical sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- Remimazolam attenuates myocardial ischemia/reperfusion injury by inhibiting ferroptosis involving the AKT/SLC7A11/GPX4 axis.International journal of molecular medicine · 2026Article
- The Wound-Heart Axis: Can Chronic Wounds Contribute to Cardiac Dysfunction?International journal of molecular sciences · 2026Review
- Sigma-1 receptor agonist SA4503 improves cerebral protective effects in an extracorporeal cardiopulmonary resuscitation rat model.JTCVS open · 2026Article
- Ferroptosis in cardiovascular diseases: molecular mechanisms and a novel therapeutic target.Molecular biomedicine · 2026Review
- Ningxue Shengban decoction containing serum alleviates immune thrombocytopenia by modulating CD4Stem cell research & therapy · 2026Article
- Role of Copper Homeostasis and Cuproptosis in Cardiovascular Disease: Molecular Insights and Metabolic Perspectives.International journal of biological sciences · 2026Review
- Ferroptosis in Cardiovascular Diseases and Ferroptosis-Related Intervention Approaches.Cardiovascular drugs and therapy · 2025Review
- The interaction between ferroptosis and myocardial ischemia-reperfusion injury: molecular mechanisms and potential therapeutic targets.European journal of medical research · 2025Review
- Epigenetic regulation and post-translational modifications of ferroptosis-related factors in cardiovascular diseases.Clinical epigenetics · 2025Review
- The diagnostic and prognostic value of serum miR-199a-5p combined with echocardiography in acute myocardial infarction.Journal of cardiothoracic surgery · 2025Article
- Ferroptosis: The Pivotal Link in Cardiovascular Diseases Pathogenesis and Therapy.International journal of general medicine · 2025Review
- Dissecting the opposing regulatory functions of endogenous nitric oxide production in colorectal cancer initiation, adaptive immune response alterations, and ferroptosis execution.Oncology reviews · 2025Review
- Noncoding RNAs regulating ferroptosis in cardiovascular diseases: novel roles and therapeutic strategies.Molecular and cellular biochemistry · 2024Review
- Ferroptosis mechanisms and regulations in cardiovascular diseases in the past, present, and future.Cell biology and toxicology · 2024Review
- Ferroptosis, a Regulated Form of Cell Death, as a Target for the Development of Novel Drugs Preventing Ischemia/Reperfusion of Cardiac Injury, Cardiomyopathy and Stress-Induced Cardiac Injury.International journal of molecular sciences · 2024Review
- Ferroptosis in cardiovascular diseases: role and mechanism.Cell & bioscience · 2023Review
- Targeting epigenetic and posttranslational modifications regulating ferroptosis for the treatment of diseases.Signal transduction and targeted therapy · 2023Review
- The mechanism of ferroptosis and its related diseases.Molecular biomedicine · 2023Review
- MiR-199a-5p promotes ferroptosis-induced cardiomyocyte death responding to oxygen-glucose deprivation/reperfusion injury via inhibiting Akt/eNOS signaling pathway.The Kaohsiung journal of medical sciences · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial ischemia/reperfusion (I/R) injury is associated with the poor outcome and higher mortality after myocardial infarction. Recent studies have revealed that miR-199a-5p participates in the process of myocardial I/R injury, but the precise roles and molecular mechanisms of miR-199a-5p in myocardial I/R injury remain not well-studied. Ferroptosis has been proposed to promote cardiomyocyte death, closely associated with myocardial I/R injury. Herein, the present study aimed to explore the function and mechanisms by which miR-199a-5p regulates whether miR-199a-5p contributes to ferroptosis-induced cardiomyocyte death responding to oxygen-glucose deprivation/reoxygenation (OGD/R) injury, an in vitro model of myocardial I/R injury focusing on Akt/eNOS signaling pathway. The results found that ferroptosis-induced cardiomyocyte death occurs and is accompanied by an increase in miR-199a-5p level in OGD/R-treated H9c2 cells. MiR-199a-5p inhibitor ameliorated ferroptosis-induced cardiomyocyte death as evidenced by the increased cell viability, the reduced reactive oxygen species (ROS) generation, lactate dehydrogenase (LDH) activity, malondialdehyde (MDA) and Fe
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