Dysregulation of Histone Acetyltransferases and Deacetylases in Cardiovascular Diseases

Figure 3

The protective effect of HDAC inhibitors in cardiac remodeling. Many risk factors such as high glucose (HG), myocardial infarction (MI), hypertension (HP), hyperlipidaemia (HLP), genetic causes (cardiomyopathy), obesity, and aging cause cardiac injury, activate pathological cellular processes (inflammation, apoptosis, oxidative stress, and fibrosis), and induce cardiac hypertrophy, remodeling, and dysfunction. HDAC inhibitors are capable of blocking elements of these detrimental biological processes and preserving cardiac function. The HDAC inhibitors, trichostatin A (TSA), suberoylanilide hydroxamic acid (SAHA), valproic acid (VPA), scriptaid, and apicidin-derivative (Api-D) have been tested in rodent heart failure models.