Table 2.

NOX4 in cardiac disease models.

NOX4 modification (cardiac disease models)	Disease model	Reported outcome	Reference
Cardiomyocyte-specific overexpression	Pressure overload	Reduced fibrosis and levels of hypertrophy	(13)
Global deletion	Pressure overload	Contractile dysfunction, severe dilatation, increased levels of hypertrophy	(13)
Cardiomyocyte-specific deletion	Pressure overload	Reduced levels of hypertrophy, fibrosis and cell death	(14)
Cardiomyocyte-specific deletion	Pressure overload	Increased levels of hypertrophy and fibrosis, diminished angiogenesis, contractile dysfunction	(15)
Endothelial-specific deletion	Pressure overload	Increased levels of hypertrophy and fibrosis, contractile dysfunction	(15)
Cardiomyocyte-specific overexpression	Pressure overload	Reprogramming of cardiac metabolism to fully maintain energetic status	(63)
Global deletion	Ischemia/reperfusion	No NOX4-dependent effects	(19)
Global deletion	Ischemia/reperfusion	Severe cardiac lesions	(21)
Cardiomyocyte-specific overexpression	Permanent left anterior descending ligation	Improved contractile function, reduced cardiac remodeling	(64)
Cardiomyocyte-specific deletion	Ischemia/reperfusion	Decreased myocardial damage, reduced ROS production, attenuation of infarct size	(20)