Non-ion channel therapeutics for heart failure and atrial fibrillation: Are CaMKII inhibitors ready for clinical use?

Eleonora Grandi, Dobromir Dobrev

Research output: Contribution to journalArticle

7 Scopus citations

Abstract

The Ca2+-calmodulin dependent protein kinase II (CaMKII) is an established central mediator of electrophysiological and contractile responses to cardiac stress, and its hyper-activation in cardiac diseases has been linked to heart failure (HF) and arrhythmia. Here we summarize the evidence supporting the role of CaMKII as a critical nodal point for therapeutic intervention against HF and atrial and ventricular tachyarrhythmias. Targeting of CaMKII in heart with inhibitors possessing appropriate selectivity might represent a novel therapeutic approach for HF and arrhythmias.

Original languageEnglish (US)
JournalJournal of Molecular and Cellular Cardiology
DOIs
StateAccepted/In press - Jan 1 2017

Keywords

  • Arrhythmia
  • Atrial fibrillation
  • CaMKII
  • Heart failure
  • Small molecules

ASJC Scopus subject areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine

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