Effect and mechanism of circHMGA2 on ferroptosis and pyroptosis in myocardial ischemia-reperfusion model CircHMGA2 exacerbates MI/R injury

Myocardial ischemia-reperfusion (MI/R) injury is a common and serious complication following reperfusion treatment for myocardial infarction (MI). Increasing evidence has verified the crucial role of circular RNAs (circRNAs) in MI/R processes. The objective this study was to investigate effects potential regulatory mechanisms circHMGA2 on injury. Hypoxia/reoxygenation (H/R) models were established using human cardiac myocytes (HCMs) mice induced by MI/R. level detected RT-qPCR. function evaluated hemodynamic parameters, activity serum enzymes, HE staining TUNEL assays. Cell proliferation measured CCK-8 assay. ferrous ion (Fe2+) determined with an iron assay kit. Ferroptosis- pyroptosis-related proteins western blotting. levels oxidative stress inflammatory factors analyzed DCFH-DA or ELISA CircHMGA2 upregulated H/R-induced HCMs tissues mice. In vitro, knockdown attenuated inhibition, restrained ferroptosis pyroptosis HCMs. This mechanism may be associated suppression NLRP3 pathway. vivo, depletion tissue damage through inhibiting pyroptosis. Taken together, enhanced via promoting pyroptosis, providing new insights into