Redox sensitive signaling pathways in cardiac remodeling, hypertrophy and failure

被引:61
作者
Anilkumar, Narayana [1 ]
Sirker, Alexander [1 ]
Shah, Ajay M. [1 ]
机构
[1] Kings Coll London, Sch Med, Dept Cardiol, James Black Ctr,Div Cardiovasc, 125 Coldharbour Lane, London SE5 9NU, England
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2009年 / 14卷
关键词
NADPH Oxidase; Nox2; Nox4; Redox signaling; Cardiac remodeling; Hypertrophy; Review; SMOOTH-MUSCLE-CELLS; INDUCED CARDIOMYOCYTE HYPERTROPHY; NEONATAL-RAT CARDIOMYOCYTES; HUMAN HEART-FAILURE; MATRIX-METALLOPROTEINASE ACTIVITY; MITOCHONDRIAL OXIDATIVE STRESS; NOX2-CONTAINING NADPH OXIDASE; NECROSIS-FACTOR-ALPHA; II-INDUCED APOPTOSIS; FACTOR-KAPPA-B;
D O I
10.2741/3443
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Adaptation of the heart to intrinsic and external stress involves complex modifications at the molecular and cellular level that lead to tissue remodeling and functional compensation or failure depending upon the nature, intensity and chronicity of the stress. Signaling mechanisms mediated by reactive oxygen species (ROS) are now known to play important roles in many aspects of this complex process. In particular, the tightly regulated generation of ROS by NADPH oxidases appears especially important in key signaling events that drive the development of cardiomyocyte hypertrophy, fibrosis, extracellular matrix remodelling and cell apoptosis. This review discusses the signaling pathways modulated by ROS during the development of cardiac remodelling and failure with a particular emphasis on the role of NADPH oxidases.
引用
收藏
页码:3168 / 3187
页数:20
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