Table 1.

Cardiac phenotype of genetically modified HDAC mice.

HDAC Class	Role in Heart	Phenotype of Mice Models
I
HDAC 1 and HDAC2	unclear	Trivedi et al. described that cardiac-specific double knock-out Hdac1/2 mice have dilated cardiomyopathy, arrhythmias, and neonatal lethality, accompanied by up-regulation of genes encoding skeletal muscle-specific myofibrillar proteins and calcium channels. Montogomery et al. did not detect any alteration of cardiac function of knock-out mice (see text).
II
HDAC 5	anti-hypertrophic	Major sensibility to the development of cardiac hypertrophy and a failure in responding to pro-hypertrophy stimuli, such as TAC and calcineurin activation.
HDAC 9	anti-hypertrophic	Major sensibility to the development of cardiac hypertrophy and a failure in responding to pro-hypertrophy stimuli, such as TAC and calcineurin activation.
III
SIRT6	anti-hypertrophic	Cardiac-specific double knock-out Sirt6 mice developed cardiac hypertrophy and heart failure; Sirt6 transgenic mice were protected from hypertrophic stimuli, such as TAC and isoproterenol infusion.
SIRT3	anti-hypertrophic	Sirt3 knock-out mice had an increased heart weight/body weight (HW/BW) ratio and interstitial fibrosis at 8 weeks of age; cardiac-specific Sirt3 transgenic mice were protected from hypertrophic stimuli, such angiotensin II infusion and isoproterenol infusion.