Literature DB >> 26475411

Oxidant stress promotes disease by activating CaMKII.

Mark E Anderson1.   

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.
Copyright © 2015 Elsevier Ltd. All rights reserved.

Entities:  

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

Mesh:

Substances:

Year:  2015        PMID: 26475411      PMCID: PMC5075238          DOI: 10.1016/j.yjmcc.2015.10.014

Source DB:  PubMed          Journal:  J Mol Cell Cardiol        ISSN: 0022-2828            Impact factor:   5.000


  60 in total

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  40 in total

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10.  Trpm2 enhances physiological bioenergetics and protects against pathological oxidative cardiac injury: Role of Pyk2 phosphorylation.

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