氧化应激通过激活钙调蛋白激酶II促进疾病发生。
Oxidant stress promotes disease by activating CaMKII.
作者信息
Anderson Mark E
机构信息
Johns Hopkins Department of Medicine, Johns Hopkins School of Medicine, Baltimore, MD 21287, United States.
出版信息
J Mol Cell Cardiol. 2015 Dec;89(Pt B):160-7. doi: 10.1016/j.yjmcc.2015.10.014. Epub 2015 Oct 22.
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.
摘要
钙/钙调蛋白依赖性蛋白激酶II（CaMKII）通过位于调节结构域的甲硫氨酸残基氧化而被激活。氧化型CaMKII（ox-CaMKII）现在被认为参与心血管疾病、肺部疾病和癌症。这篇特邀综述总结了目前关于ox-CaMKII在疾病中作用的证据，考虑了关键的知识空白，并提出了新的研究领域。
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