Oxidant stress promotes disease by activating CaMKII

Mark E. Anderson

Research output: Contribution to journalReview articlepeer-review

56 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)160-167
Number of pages8
JournalJournal of Molecular and Cellular Cardiology
StatePublished - Dec 1 2015


  • Asthma
  • Atherosclerosis
  • Atrial fibrillation
  • CaMKII
  • Cancer
  • Heart failure
  • MsrA
  • Myocardial infarction
  • Sinus node dysfunction
  • Vascular smooth muscle
  • ox-CaMKII

ASJC Scopus subject areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine


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