βIIPKC and εPKC isozymes as potential pharmacological targets in cardiac hypertrophy and heart failure

被引：47

作者：

Batista Ferreira, Julio Cesar ^{[1
,2
]}

Brum, Patricia Chakur ^{[2
]}

Mochly-Rosen, Daria ^{[1
]}

机构：

[1] Stanford Univ, Sch Med, Dept Chem & Syst Biol, CCSR, Stanford, CA 94305 USA

[2] Univ Sao Paulo, Sch Phys Educ & Sport, BR-05508900 Sao Paulo, Brazil

来源：

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY | 2011年 / 51卷 / 04期

基金：

巴西圣保罗研究基金会;

关键词：

PKC signaling pathways; Cardiac remodeling; Heart failure; PROTEIN-KINASE-C; ISOFORM EXPRESSION; DELTA-PKC; DIFFERENTIAL ACTIVATION; VENTRICULAR HYPERTROPHY; SUDDEN-DEATH; RAT; INHIBITION; ALPHA; HYPERTENSION;

D O I：

10.1016/j.yjmcc.2010.10.020

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Cardiac hypertrophy is a complex adaptive response to mechanical and neurohumoral stimuli and under continual stressor, it contributes to maladaptive responses, heart failure and death. Protein kinase C (PKC) and several other kinases play a role in the maladaptative cardiac responses, including cardiomyocyte hypertrophy, myocardial fibrosis and inflammation. Identifying specific therapies that regulate these kinases is a major focus of current research. PKC, a family of serine/threonine kinases, has emerged as potential mediators of hypertrophic stimuli associated with neurohumoral hyperactivity in heart failure. In this review, we describe the role of PKC isozymes that is involved in cardiac hypertrophy and heart failure. This article is part of a special issue entitled "Key Signaling Molecules in Hypertrophy and Heart Failure". (C) 2010 Elsevier Ltd. All rights reserved.

引用

页码：479 / 484

页数：6

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