Oxidant stress promotes disease by activating CaMKII

J Mol Cell Cardiol. 2015 Dec;89(Pt B):160-7. doi: 10.1016/j.yjmcc.2015.10.014. Epub 2015 Oct 22.

Abstract

CaMKII is activated by oxidation of methionine residues residing in the regulatory domain. Oxidized CaMKII (ox-CaMKII) is now thought to participate in cardiovascular and pulmonary diseases and cancer. This invited review summarizes current evidence for the role of ox-CaMKII in disease, considers critical knowledge gaps and suggests new areas for inquiry.

Keywords: Asthma; Atherosclerosis; Atrial fibrillation; CaMKII; Cancer; Heart failure; MsrA; Myocardial infarction; Sinus node dysfunction; Vascular smooth muscle; ox-CaMKII.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2 / chemistry
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2 / metabolism*
  • Cell Death / drug effects
  • Humans
  • Molecular Sequence Data
  • Oxidants / toxicity*
  • Oxidative Stress / drug effects*
  • Reactive Oxygen Species / metabolism
  • Vascular Diseases / enzymology*
  • Vascular Diseases / pathology*

Substances

  • Oxidants
  • Reactive Oxygen Species
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2