Role of CR6-Interacting Factor 1 (Crif1) in Cardiac Mitochondrial Structure and Stress-Induced Functional Decline

BACKGROUND AND OBJECTIVES: in regulating mitochondrial function in the heart. METHODS: knock-down mice using a Myh6-Cre system. Mitochondrial function was assessed by measuring oxygen consumption rates. Histological and echocardiographic examinations were performed at baseline and 2 weeks after isoproterenol infusion. RESULTS: knock-down resulted in mitochondrial dysfunction, the cardiac phenotype remained normal showing preserved ejection fraction (EF) and fractional shortening (FS). However, cardiac dysfunction was aggravated under isoproterenol-induced stress, resulting in a decreased EF and FS. Cardiac hypertrophy, a typical adaptive response to isoproterenol stimulation, was attenuated. CONCLUSIONS: is critical for maintaining the structure and function of mitochondria in cardiomyocytes. Additionally, mitochondrial abnormalities in the heart impair stress adaptation, leading to aggravated cardiac dysfunction under stress.