Oxidant stress promotes disease by activating CaMKII

被引：92

作者：

Anderson, Mark E. ^{[1
]}

机构：

[1] Johns Hopkins Sch Med, Johns Hopkins Dept Med, Baltimore, MD 21287 USA

来源：

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY | 2015年 / 89卷

基金：

美国国家卫生研究院;

关键词：

CaMKII; ox-CaMKII; MsrA; Heart failure; Myocardial infarction; Atrial fibrillation; Sinus node dysfunction; Atherosclerosis; Vascular smooth muscle; Asthma; Cancer; PROTEIN-KINASE-II; ACUTE MYOCARDIAL-INFARCTION; BASE-LINE CHARACTERISTICS; SINUS NODE DYSFUNCTION; CARDIAC-HYPERTROPHY; BETA-CAROTENE; LUNG-CANCER; MECHANISM; DELTA; INHIBITION;

D O I：

10.1016/j.yjmcc.2015.10.014

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

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. (C) 2015 Elsevier Ltd. All rights reserved.

引用

页码：160 / 167

页数：8

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