Table 1.

Summary of mitophagy pathways in cardiac diseases.

Pathology	Mechanism of action
Ischemic heart disease	The ablation of PINK1 in mice induced cardiac hypertrophy at 2 months of age, and PINK1 knockout aggravated infarct size after I/R injury
	During I/R injury, BNIP3 is upregulated and FUNDC1 is downregulated
	Fundc1-knockout (KO) platelets present impaired mitochondria, which cause more I/R heart injury
	The depletion of Pgam5 in mice showed augmented infarct volume, well correlated with mitophagy inhibition
Diabetic cardiomyopathy	Mitochondrial ROS production was elevated, and BNIP3 level was inhibited in prediabetic rats
	PINK1 and Parkin levels were suppressed in both type 1 and type 2 diabetes models. Parkin ablation mice displayed enhanced mitophagy and serious cardiac hypertrophy under high-fat diet stress
	TAT-Beclin1 contributed to the suppression of cardiomyopathy development
Cardiac hypertrophy	Parkin-depleted mice exhibited elevated cardiac remodeling, and PINK1-ablated mice showed abnormal mitochondrial function, increased oxidative stress, and pathological hypertrophy
	The depletion of BNIP3 also exhibited cardiac hypertrophy at old age
Heart failure	Beclin1 and LC3-II were reduced in the specimen of HF patients
	MFN2 is reported to modulate HF-associated mitophagy via changing the mitochondrial membrane potential
	PINK1 downregulation is commonly observed in HF patients. PINK1-depleted mice were more liable to heart stress and heart failure induced by overload
	NIX depletion showed decreased myocardial fibrosis and more normal systolic function in stress-induced HF mice models
	BNIP3 is activated under hypoxia condition and elevated in an in vitro model of chronic HF
Arrhythmia	Decrease in mitophagy leads to proarrhythmic spontaneous Ca2+ release via oxidized RyR2s by mito-ROS