Protein kinase C mechanisms that contribute to cardiac remodelling

被引:43
作者
Newton, Alexandra C. [1 ]
Antal, Corina E. [1 ,2 ]
Steinberg, Susan F. [3 ]
机构
[1] Univ Calif San Diego, Dept Pharmacol, La Jolla, CA 92093 USA
[2] Univ Calif San Diego, Biomed Sci Grad Program, La Jolla, CA 92093 USA
[3] Columbia Univ, Dept Pharmacol, New York, NY 10032 USA
基金
美国国家卫生研究院;
关键词
myocardial remodelling; post translational modification; protein kinase C; PHOSPHOINOSITIDE-DEPENDENT KINASE; ACTIVATION LOOP PHOSPHORYLATION; ALPHA PKC-ALPHA; DELTA-NULL MICE; HEART-FAILURE; IN-VIVO; BETA-II; ALZHEIMERS-DISEASE; THERAPEUTIC TARGET; ACTIVITY REPORTER;
D O I
10.1042/CS20160036
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Protein phosphorylation is a highly-regulated and reversible process that is precisely controlled by the actions of protein kinases and protein phosphatases. Factors that tip the balance of protein phosphorylation lead to changes in a wide range of cellular responses, including cell proliferation, differentiation and survival. The protein kinase C (PKC) family of serine/threonine kinases sits at nodal points in many signal transduction pathways; PKC enzymes have been the focus of considerable attention since they contribute to both normal physiological responses as well as maladaptive pathological responses that drive a wide range of clinical disorders. This review provides a background on the mechanisms that regulate individual PKC isoenzymes followed by a discussion of recent insights into their role in the pathogenesis of diseases such as cancer. We then provide an overview on the role of individual PKC isoenzymes in the regulation of cardiac contractility and pathophysiological growth responses, with a focus on the PKC-dependent mechanisms that regulate pump function and/or contribute to the pathogenesis of heart failure.
引用
收藏
页码:1499 / 1510
页数:12
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