MiR ‐199a‐5p promotes ferroptosis‐induced cardiomyocyte death responding to oxygen–glucose deprivation/reperfusion injury via inhibiting Akt/ eNOS signaling pathway
Author:
Affiliation:
1. Department of Cardiovascular Center, Beijing Tongren Hospital Capital Medical University Beijing China
Publisher
Wiley
Subject
General Medicine
Link
https://onlinelibrary.wiley.com/doi/pdf/10.1002/kjm2.12605
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2. ALKBH5‐mediated m6A demethylation of pri‐miR‐199a‐5p exacerbates myocardial ischemia/reperfusion injury by regulating TRAF3‐mediated pyroptosis;Journal of Biochemical and Molecular Toxicology;2024-04
3. Ferroptosis mechanisms and regulations in cardiovascular diseases in the past, present, and future;Cell Biology and Toxicology;2024-03-21
4. 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;2024-01-11
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