Is CaMKII a link between inflammation and hypertrophy in heart?

Madhu V. Singh, Mark E. Anderson

Research output: Contribution to journalReview article

Abstract

Myocardial infarction is a major cause of morbidity and mortality in the developing and developed world. Although current interventions have been successful in prolonging life, they are inadequate because mortality is still high among MI patients. The multifunctional Ca2+/calmodulin-dependent protein kinase (CaMKII) plays a key role in the structure and contractility of the myocardium. CaMKII activity is increased in MI hearts and CaMKII promotes cardiac hypertrophy and inflammation, processes consistently activated by myocardial injury. Hypertrophy and inflammation are also related to neurohumoral and redox signaling which uncouple CaMKII activation from Ca 2+/calmodulin dependence. Thus, CaMKII may act as a nodal point for integrating hypertrophic and inflammatory signaling in myocardium.

Original languageEnglish (US)
Pages (from-to)537-543
Number of pages7
JournalJournal of Molecular Medicine
Volume89
Issue number6
DOIs
StatePublished - Jun 1 2011
Externally publishedYes

Keywords

  • AngII
  • CaMKII
  • Heart
  • Heart attack
  • Hypertrophy
  • Inflammation
  • Myocardial infarction
  • Myocardium
  • Oxidative stress
  • ROS
  • Toll-like receptors

ASJC Scopus subject areas

  • Molecular Medicine
  • Drug Discovery
  • Genetics(clinical)

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