Table 1.

Mouse models implicating autophagy involvement in cardiovascular diseases

Disease model	Genetic Intervention in mice	Results	Ref
Aging	Atg5 transgene (Tg) overexpression	Reduced age-related cardiac fibrosis, increased lifespan extension	(Pyo et al., 2013)
	BECN1F121A knockin	Reduced age-associated cardiac alterations, increased lifespan	(Fernández et al., 2018)
	Prkn Tg overexpression	Reduced age-associated cardiac abnormalities	(Hoshino et al., 2013)
Atherosclerosis	atg5 −/−	Accelerated atherosclerosis	(Liao et al., 2012b)
Cardiomyopathy	Atg5 +/−	Exacerbated cardiac hypertrophy	(Zhao et al., 2014)
	Atg7 Tg overexpression	Reduced cardiac hypertrophy, limited intracellular protein aggregation, and increased mouse survival	(Bhuiyan et al., 2013)
	Becn1 +/−	Accelerated heart failure	(Tannous et al., 2008)
	Becnl Tg overexpression	Exacerbated pathogenic remodeling	(Zhu et al., 2007)
Myocardial infarction	Becn1 +/−	Reduced cardiac damage at reperfusion	(Matsui et al., 2007)
	prkn −/− prkn −/−	Exacerbated cardiac injury and reduced survival Increased infarct size, hypertrophy	(Kubli et al., 2013)
	atg5 −/−	Increased sensitivity, exacerbated hypertrophy	(Nakai et al., 2007)
I/R injury	Becn1 +/−	Cardioprotective during reperfusion	(Matsui et al., 2007)
Pressure overload	atg5 −/−	Increased sensitivity, exacerbated hypertrophy	(Nakai et al., 2007)
	Becn1+/− Becn1 Tg overexpression	Reduced pathological cardiac remodeling Exacerbated pathological cardiac remodeling	(Zhu et al., 2007)
Sepsis	Becn1 +/−	Cardioprotective during reperfusion	(Sun et al., 2018)