Table 1.

The physiological role of class I and class IIa HDACs in cardiac development and heart diseases.

HDAC subtype	Model	Phenotype	Disease functions in the heart	References
HDAC1	P19CL16 cells	Differentiation	HDAC1 protein was decreased during cardiomyogenesis	Liu et al. [23]
	HDAC1-deficient mice	Proliferation	Embryo lethality because of proliferation defects	Lagger et al. [24], Montgomery et al. [25]
HDAC2	HDAC2 knockout mice	Proliferation	Proliferation rates of cardiac myocytes in HDAC2 knockout mice were elevated	Trivedi et al. [26]
	HDAC2 knockout mice	Proliferation	Increase in proliferation at P1Lethality after P1	Montgomery et al. [25]
	HDAC2 knockout mice	Hypertrophy	HDAC2 knockout mice are resistant to cardiac hypertrophy	Trivedi et al. [26]
	HDAC2 transgenic mice	Hypertrophy	HDAC2 transgenic mice show cardiac hypertrophy	Trivedi et al. [26]
	Aortic banding mice	Hypertrophy	HDAC2 and HSP70 cause cardiac hypertrophy	Kee et al. [14]
	Hsp70 knockout mice
HDAC3	HDAC3 transgenic mice	Proliferation	HDAC3 transgenic mice show postnatal cardiac myocyte proliferation	Trivedi et al. [27]
	HDAC3 knockout mice	Hypertrophy	HDAC3 knockout mice show massive cardiac hypertrophy	Montgomery et al. [28]
	HDAC3 knockout mice	Metabolism	HDAC3 regulates cardiac energy metabolism	Montgomery et al. [28]
HDAC4	HDAC4 knockout mice		HDAC4 knockout mice die perinatally because of abnormal chondrocyte hypertrophy	Vega et al. [29]
HDAC5	HDAC5 knockout mice	Hypertrophy	Mice lacking HDAC5 develop enlarged hearts in response to pressure overload	Chang et al. [30]
HDAC9	HDAC9 knockout mice	Hypertrophy	HDAC9 mutant mice develop cardiac hypertrophy	Zhang et al. [31]