Review Article
Roles and Targets of Class I and IIa Histone Deacetylases in Cardiac Hypertrophy
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] |
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