title: Oxidant stress promotes disease by activating CaMKII.
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.
authors.affiliation: Johns Hopkins Department of Medicine, Johns Hopkins School of Medicine, Baltimore, MD 21287, United States. Electronic address: mark.anderson@jhmi.edu.
authors.forename: Mark E
authors.initials: ME
authors.lastname: Anderson
mesh_terms: D000595:Amino Acid Sequence; D000818:Animals; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2 / Q000737:chemistry / Q000378:metabolism*; D016923:Cell Death / Q000187:drug effects; D006801:Humans; D008969:Molecular Sequence Data; D016877:Oxidants / Q000633:toxicity*; D018384:Oxidative Stress / Q000187:drug effects*; D017382:Reactive Oxygen Species / Q000378:metabolism; D014652:Vascular Diseases / Q000201:enzymology* / Q000473:pathology*
chemical_list: D016877:Oxidants; D017382:Reactive Oxygen Species; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2
keywords: Asthma; Atherosclerosis; Atrial fibrillation; CaMKII; Cancer; Heart failure; MsrA; Myocardial infarction; Sinus node dysfunction; Vascular smooth muscle; ox-CaMKII