ArticleOpen medicine (Warsaw, Poland)2026
ID2 attenuates post-MI ventricular arrhythmias by targeting GATA4 suppression to preserve mitochondrial function and Na
Article in Open medicine (Warsaw, Poland), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objectives: Post-myocardial infarction (MI) ventricular arrhythmia (VA) remains a leading cause of sudden cardiac death. Current antiarrhythmic drugs often fail to target the core metabolic-structural remodeling underlying arrhythmias. The transcriptional repressor ID2, which has been implicated in cardiovascular development, remains poorly characterized regarding its role and contribution to VA pathogenesis. This study investigated the role of the transcriptional repressor ID2 in post-myocardial infarction ventricular arrhythmia. Methods: An MI rat model was established via left anterior descending (LAD) coronary artery ligation. ID2 expression in myocardial tissues was quantified by immunofluorescence and western blot. Flow cytometry and biochemical assays were employed to evaluate the impact of ID2 modulation on arrhythmogenesis. Hypoxia-challenged cardiomyocytes treated with rotenone (Complex I inhibitor) and digoxin (Na Results: ID2 expression was significantly downregulated in MI rats and was inversely correlated with PVC frequency and VT/VF duration. Overexpression of ID2 reduced arrhythmia severity scores and attenuated PVC/VT/VF incidence in MI rats; me'anwhile, it ameliorated mitochondrial dysfunction, as reflected by restored membrane potential and ATP levels and reduced ROS, and improved Na Conclusions: This study demonstrates that ID2 alleviates VA by suppressing GATA4 expression, thereby mitigating mitochondrial dysfunction and Na
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