Ablation of Mitophagy Receptor FUNDC1 Accentuates Septic Cardiomyopathy through ACSL4-Dependent Regulation of Ferroptosis and Mitochondrial Integrity

Sepsis evokes compromised myocardial function prompting heart failure albeit target therapy remains dismal. Our study examined the possible role of mitophagy receptor FUNDC1 in septic cardiomyopathy. A sepsis model was established using cecal ligation and puncture (CLP) in FUNDC1 knockout (FUNDC1