Literature DB >> 18171314

Histone deacetylase inhibition in the treatment of heart disease.

Jeff M Berry1, Dian J Cao, Beverly A Rothermel, Joseph A Hill.   

Abstract

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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Year:  2008        PMID: 18171314     DOI: 10.1517/14740338.7.1.53

Source DB:  PubMed          Journal:  Expert Opin Drug Saf        ISSN: 1474-0338            Impact factor:   4.250


  20 in total

1.  Histone deacetylase inhibition blunts ischemia/reperfusion injury by inducing cardiomyocyte autophagy.

Authors:  Min Xie; Yongli Kong; Wei Tan; Herman May; Pavan K Battiprolu; Zully Pedrozo; Zhao V Wang; Cyndi Morales; Xiang Luo; Geoffrey Cho; Nan Jiang; Michael E Jessen; John J Warner; Sergio Lavandero; Thomas G Gillette; Aslan T Turer; Joseph A Hill
Journal:  Circulation       Date:  2014-01-06       Impact factor: 29.690

Review 2.  Inhibition of hypertrophy is a good therapeutic strategy in ventricular pressure overload.

Authors:  Gabriele G Schiattarella; Joseph A Hill
Journal:  Circulation       Date:  2015-04-21       Impact factor: 29.690

Review 3.  The nonepigenetic role for small molecule histone deacetylase inhibitors in the regulation of cardiac function.

Authors:  Samantha S Romanick; Bradley S Ferguson
Journal:  Future Med Chem       Date:  2019-06-04       Impact factor: 3.808

Review 4.  Autophagy as a therapeutic target in cardiovascular disease.

Authors:  Andriy Nemchenko; Mario Chiong; Aslan Turer; Sergio Lavandero; Joseph A Hill
Journal:  J Mol Cell Cardiol       Date:  2011-06-23       Impact factor: 5.000

5.  HDACs and hypertrophy, kinases and cancer.

Authors:  Berdymammet Hojayev; Joseph A Hill
Journal:  Circulation       Date:  2011-05-16       Impact factor: 29.690

6.  Histone deacetylase (HDAC) inhibitors attenuate cardiac hypertrophy by suppressing autophagy.

Authors:  Dian J Cao; Zhao V Wang; Pavan K Battiprolu; Nan Jiang; Cyndi R Morales; Yongli Kong; Beverly A Rothermel; Thomas G Gillette; Joseph A Hill
Journal:  Proc Natl Acad Sci U S A       Date:  2011-02-18       Impact factor: 11.205

7.  Diminished cardiac fibrosis in heart failure is associated with altered ventricular arrhythmia phenotype.

Authors:  Jorge Massare; Jeff M Berry; Xiang Luo; Farhana Rob; Janet L Johnstone; John M Shelton; Rhonda Bassel-Duby; Joseph A Hill; R Haris Naseem
Journal:  J Cardiovasc Electrophysiol       Date:  2010-09

8.  Hypothesis: role for ammonia neutralization in the prevention and reversal of heart failure.

Authors:  Oscar H L Bing
Journal:  Am J Physiol Heart Circ Physiol       Date:  2018-03-16       Impact factor: 4.733

Review 9.  Roles and targets of class I and IIa histone deacetylases in cardiac hypertrophy.

Authors:  Hae Jin Kee; Hyun Kook
Journal:  J Biomed Biotechnol       Date:  2010-11-29

10.  Nitric oxide and histone deacetylases: A new relationship between old molecules.

Authors:  P Marc D Watson; Antonella Riccio
Journal:  Commun Integr Biol       Date:  2009
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