HDAC-dependent ventricular remodeling

Min Xie, Joseph A Hill

Research output: Contribution to journalReview article

57 Scopus citations

Abstract

Heart failure, a syndrome culminating the pathogenesis of many forms of heart disease, is highly prevalent and projected to be increasingly so for years to come. Major efforts are directed at identifying the means of preventing, slowing, or possibly reversing the unremitting progression of pathological stress leading to myocardial injury and ultimately heart failure. Indeed, despite widespread use of evidence-based therapies, heart failure morbidity and mortality remain high. Recent work has uncovered a fundamental role of reversible protein acetylation in the regulation of many biological processes, including pathological remodeling of the heart. This reversible acetylation is governed by enzymes that attach (histone acetyltransferases, HATs) or remove (histone deacetylases, HDACs) acetyl groups. In the latter case, small molecule inhibitors of HDACs are currently being tested for a variety of oncological indications. Now, evidence has revealed that HDAC inhibitors blunt pathological cardiac remodeling in the settings of pressure overload and ischemia/reperfusion, thereby diminishing the emergence of heart failure. Mechanistically, HDAC inhibitors reduce stress-induced cardiomyocyte death, hypertrophy, and ventricular fibrosis. Looking to the future, HDAC inhibitor therapy may emerge as a novel means of arresting the untoward consequences of pathological cardiac stress, conferring clinical benefit to millions of patients with heart failure.

Original languageEnglish (US)
Pages (from-to)229-235
Number of pages7
JournalTrends in Cardiovascular Medicine
Volume23
Issue number6
DOIs
StatePublished - Aug 1 2013

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Fingerprint Dive into the research topics of 'HDAC-dependent ventricular remodeling'. Together they form a unique fingerprint.

  • Cite this