Is CaMKII a link between inflammation and hypertrophy in heart?

J Mol Med (Berl). 2011 Jun;89(6):537-43. doi: 10.1007/s00109-011-0727-5. Epub 2011 Jan 29.


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 Ca(2+)/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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2 / metabolism*
  • Cardiomegaly / metabolism
  • Cardiomegaly / pathology
  • Cardiomegaly / physiopathology*
  • Heart / physiopathology
  • Humans
  • Inflammation / physiopathology*
  • Mice
  • Myocardial Infarction / physiopathology
  • Myocardium / metabolism
  • NF-kappa B / metabolism
  • Oxidative Stress
  • Reactive Oxygen Species / metabolism
  • Signal Transduction
  • Toll-Like Receptors / metabolism


  • NF-kappa B
  • Reactive Oxygen Species
  • Toll-Like Receptors
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2