Mechanisms of Disease: Ion channel remodeling in the failing ventricle

Robert D. Nass, Takeshi Aiba, Gordon F. Tomaselli, Fadi G. Akar

Research output: Contribution to journalReview article

81 Scopus citations

Abstract

In an attempt to compensate for compromised hemodynamics in heart failure, neurohumoral mechanisms are activated that trigger fundamental changes in gene expression and in protein processing, trafficking and post-translational regulation, resulting in myocyte hypertrophy. Unfortunately, over time these changes become maladaptive, predisposing to myocyte loss, chamber dilatation, interstitial hyperplasia and intercellular uncoupling. Intrinsic and peripheral responses to mechanical dysfunction alter the expression and function of key ion channels and calcium-handling proteins, thereby remodeling the cellular action potential and the intracellular calcium transient. This electrophysiological remodeling renders the heart more vulnerable to ventricular arrhythmias that underlie sudden cardiac death. In this Review, we consider key ventricular ionic changes that are associated with heart failure, with the intention of identifying molecular targets for antiarrhythmic therapy.

Original languageEnglish (US)
Pages (from-to)196-207
Number of pages12
JournalNature Clinical Practice Cardiovascular Medicine
Volume5
Issue number4
DOIs
StatePublished - Apr 1 2008
Externally publishedYes

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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