Table 2.

Histone modifications and therapeutic targets involved in cardiovascular diseases

Target	Epigenetic mechanisms	Condition	Organism/in vitro, in vivo	Effects	Ref.
TSA	Inhibition of HDAC4	Ischemic injury	Mouse, in vitro and in vivo	HDACi would be predicted to have a beneficial effect in the context of active ischemia	Granger et al[28] (2008)
TSA/VPA	Class I HDACs	Cardiac hypertrophy	Mouse, in vitro and in vivo	Therapeutic target for preventing or reversing cardiac hypertrophy and subsequent heart failure	Kee et al[29] (2006)
TSA	Inhibition of HDACs	Atrial fibrosis and arrhythmias	Mouse, in vitro and in vivo	Reversed myocardial fibrosis	Liu et al[30] (2008)
TSA	Inhibition of HDACs	Acute myocardial ischemia and reperfusion injury	Mouse, in vitro and in vivo	Improved cardiac functional recovery and antagonized myocardial remodeling in chronic myocardial infarction	Zhang et al[31] (2012)
TSA/SAHA	HDAC inhibitor	Myocardial infarct	Mouse, rabbit, in vivo	Reduced infarct size in a large animal model	Xie et al[35] (2014)
SAHA/sodium valproate	Inhibition of HDACs	Ischemic injury	Mouse, in vitro and in vivo	Potential therapeutic strategy for restoring compromised cardiac proteostasis	Wang et al[36] (2011)
VPA or tributyrin	Inhibition of HDACs	Infarct	Rat, in vitro	Attenuated ventricular remodeling after infarction	Lee et al[37] (2007)
MS-275A	Inhibition of class I/II HDACs	Infarct	Rat, in vivo	Significant reduction of infarct area observed	Aune et al[39] (2014)
Apicidin	Inhibition of class I HDACs	Cardiac hypertrophy and heart failure	Rat pups, in vitro Mouse, in vivo	Preserved cardiac function in the long-term	Gallo et al[42] (2008)
Curcumin	p300 HAT inhibitor	Heart failure	Rat, in vitro	Prevented deterioration of systolic function and heart failure	Morimoto et al[45] (2008)

TSA: Trichostatin A; HDAC: Histone deacetylases; HDACi: Inhibitors of histone deacetylases; SAHA: Suberoylanilide hydroxamic acid; VPA: Valproic acid.