Oxidant stress promotes disease by activating CaMKII

被引：90
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
收藏
页码：160 / 167
页数：8
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