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Is CaMKII a link between inflammation and hypertrophy in heart?
Journal article   Peer reviewed

Is CaMKII a link between inflammation and hypertrophy in heart?

Madhu Singh and Mark Anderson
Journal of molecular medicine (Berlin, Germany), Vol.89(6), pp.537-543
06/2011
DOI: 10.1007/s00109-011-0727-5
PMCID: PMC3731449
PMID: 21279501
url
https://www.ncbi.nlm.nih.gov/pmc/articles/3731449View
Open Access

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 Ca2+/calmodulin dependence. Thus, CaMKII may act as a nodal point for integrating hypertrophic and inflammatory signaling in myocardium.
Human Genetics Heart Myocardial infarction Oxidative stress Internal Medicine Inflammation Heart attack Biomedicine CaMKII ROS Myocardium Toll-like receptors Molecular Medicine AngII Hypertrophy

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