Journal
EXPERT OPINION ON DRUG SAFETY
Volume 7, Issue 1, Pages 53-67Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1517/14740338.7.1.53
Keywords
cardiac hypertrophy; fibrosis; heart failure; histone deacetylases; remodeling
Categories
Funding
- NHLBI NIH HHS [R01 HL072016] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL072016] Funding Source: NIH RePORTER
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Recent work has demonstrated the importance of chromatin remodeling, especially histone acetylation, in the control of gene expression in the heart. Studies in preclinical models suggest that inhibition of histone deacetylase (HDAC) activity - using compounds that show promise in ongoing oncology trials - blunts pathologic growth of cardiac myocytes. indeed, small-molecule inhibitors of HDACs are members of an evolving class of pharmacologic agents in development for the treatment of several diseases. If proved effective in the treatment of heart disease, HDAC inhibitors could have a significant impact on public health, as cardiovascular disease remains the leading cause of death in the US. This paper reviews understanding of the mechanisms of action of HDAC inhibitors in the heart and summarizes emerging data regarding their effects on disease-related cardiac remodeling and function.
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