Cardiac histone acetylation - Therapeutic opportunities abound

Timothy A. McKinsey, Eric N. Olson

Research output: Contribution to journalReview article

105 Scopus citations

Abstract

Diverse etiologic factors trigger a cardiac remodeling process in which the heart becomes abnormally enlarged with a consequent decline in cardiac function and eventual heart failure. Heart failure is traditionally treated with drugs that antagonize early signaling events at or near the cell membrane. Although such approaches have short-term efficacy, the five-year mortality rate for patients with late-stage heart failure continues to exceed 50%. Because of the redundant nature of the signaling networks that drive cardiac pathogenesis, targeting the common downstream elements of the cascades would be a more effective therapeutic strategy. Recent studies point to the importance of enzymes that control histone acetylation as stress-responsive regulators of gene expression in the heart. Given their role as nuclear integrators that couple divergent upstream signals to the gene program for cardiac remodeling, we propose that these chromatin-modifying factors represent auspicious targets for the pharmacological manipulation of cardiac disease.

Original languageEnglish (US)
Pages (from-to)206-213
Number of pages8
JournalTrends in Genetics
Volume20
Issue number4
DOIs
StatePublished - Apr 1 2004

ASJC Scopus subject areas

  • Genetics

Fingerprint Dive into the research topics of 'Cardiac histone acetylation - Therapeutic opportunities abound'. Together they form a unique fingerprint.

  • Cite this