Table 1. Genetically modified mice and their cardiac phenotypes.

Model	Mitophagy	Phenotypes	Ref
Parkin KO	Decreased	Increased sensitivity to MI and doxorubicin exposure, accumulation of dysfunctional mitochondria, and oxidative damage with age, reduced life span	45),52),53)
Parkin TG	Increased	Increased life span, preserved cardiac function with aging	52),54)
PINK1 KO	NA	Mitochondrial dysfunction, cardiomyopathy, increased sensitivity to I/R	43),44)
BNIP3 KO	NA	Decreased apoptosis and cardiac remodeling in response to I/R	55)
BNIP3 TG	NA	Increased sensitivity to MI, increased apoptosis	55)
NIX KO	NA	Decreased cardiac remodeling and preserved cardiac function in response to pressure overload	56)
NIX TG	NA	Ventricular dilation, reduced cardiac function	56)

Reproduced from “Mitophagy and heart failure.” By Shires and Gustafsson, Journal of Molecular Medicine 2015;93:253-62.³⁰⁾

I/R = ischemia-reperfusion; KO = knock out; MI = myocardial infarction; NA = not assessed; I/R = ischemia-reperfusion; TG = transgenic.