Moxibustion alleviates autophagy and inhibits ferroptosis to improve cardiac function in rats with post-myocardial infarction heart failure.

objectiveTo explore the mechanism by which moxibustion alleviates autophagy and inhibits ferroptosis, thereby improving myocardial fibrosis in rats with post-myocardial infarction heart failure (post-MI HF).

methodsWe used a rat model of post-MI HF rats. Interventions included moxibustion and intraperitoneal injection of rapamycin (RAPA) along with assessing echocardiography, cardiac pathology, myocardial mitochondrial morphology, co-immunofluorescence, transmission electron microscope, Western blotting, and reverse transcriptase-quantitative polymerase chain reaction.

resultsMoxibustion improves the left ventricular ejection fraction and fractional shortening, myocardial cell morphology, and myocardial fibrosis levels induced by post-MI HF. In addition, it reduces the immunofluorescence co-localization intensity of nuclear receptor coactivator 4 (NCOA4) and microtubule-associated protein 1A/1B light chain 3 and decreases the level of intracellular free iron. It suppresses autophagy and ferroptosis-related indicators, downregulates NCOA4 expression, upregulates glutathione peroxidase 4 expression, and decreases lipid peroxidation levels. The activation of autophagy increases NCOA4 expression and promotes ferroptosis. Furthermore, moxibustion counteracts the effects of RAPA.

conclusionsMoxibustion can alleviate myocardial fibrosis and exert cardioprotective effects by regulating autophagy and inhibiting ferroptosis. Our findings indicate that targeting autophagy-induced ferroptosis may serve as a novel therapeutic approach for the treatment of post-MI HF.