Redox sensitive signaling pathways in cardiac remodeling, hypertrophy and failure

被引:62
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
相关论文
共 145 条
[41]   Apoptotic cascade initiated by angiotensin II in neonatal cardiomyocytes: role of DNA damage [J].
Grishko, V ;
Pastukh, V ;
Solodushko, V ;
Gillespie, M ;
Azuma, J ;
Schaffer, S .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2003, 285 (06) :H2364-H2372
[42]   Functional association of NOX1 with P22PHOX in vascular smooth muscle cells [J].
Hanna, IR ;
Hilenski, LL ;
Dikalova, A ;
Taniyama, Y ;
Dikalov, S ;
Lyle, A ;
Qum, MT ;
Lassègue, B ;
Griendling, KK .
FREE RADICAL BIOLOGY AND MEDICINE, 2004, 37 (10) :1542-1549
[43]   Regulation of cardiac hypertrophy by intracellular signalling pathways [J].
Heineke, Joerg ;
Molkentin, Jeffery D. .
NATURE REVIEWS MOLECULAR CELL BIOLOGY, 2006, 7 (08) :589-600
[44]   Increased myocardial NADPH oxidase activity in human heart failure [J].
Heymes, C ;
Bendall, JK ;
Ratajczak, P ;
Cave, AC ;
Samuel, JL ;
Hasenfuss, G ;
Shah, AM .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2003, 41 (12) :2164-2171
[45]   Long-term inhibition of Rho-kinase suppresses angiotensin II-induced cardiovascular hypertrophy in rats in vivo - Effect on endothelial NAD(P)H oxidase system [J].
Higashi, M ;
Shimokawa, H ;
Hattori, T ;
Hiroki, J ;
Mukai, Y ;
Morikawa, K ;
Ichiki, T ;
Takahashi, S ;
Takeshita, A .
CIRCULATION RESEARCH, 2003, 93 (08) :767-775
[46]   Involvement of reactive oxygen species-mediated NF-κB activation in TNF-α-induced cardiomyocyte hypertrophy [J].
Higuchi, Y ;
Otsu, K ;
Nishida, K ;
Hirotani, S ;
Nakayama, H ;
Yamaguchi, O ;
Matsumura, Y ;
Ueno, H ;
Tada, M ;
Hori, M .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2002, 34 (02) :233-240
[47]   Distinct subcellular localizations of Nox1 and Nox4 in vascular smooth muscle cells [J].
Hilenski, LL ;
Clempus, RE ;
Quinn, MT ;
Lambeth, JD ;
Griendling, KK .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2004, 24 (04) :677-683
[48]  
Hill MF, 1996, AM J PATHOL, V148, P291
[49]   Nox2-containing NADPH oxidase and Akt activation play a key role in angiotensin II-induced cardiomyocyte hypertrophy [J].
Hingtgen, Shawn D. ;
Tian, Xin ;
Yang, Jusan ;
Dunlay, Shannon M. ;
Peek, Andrew S. ;
Wu, Yihe ;
Sharma, Ram V. ;
Engelhardt, John F. ;
Davisson, Robin L. .
PHYSIOLOGICAL GENOMICS, 2006, 26 (03) :180-191
[50]   Ca2+-sensitive tyrosine kinase Pyk2/CAK β-dependent signaling is essential for G-protein-coupled receptor agonist-induced hypertrophy [J].
Hirotani, S ;
Higuchi, Y ;
Nishida, K ;
Nakayama, H ;
Yamaguchi, O ;
Hikoso, S ;
Takeda, T ;
Kashiwase, K ;
Watanabe, T ;
Asahi, M ;
Taniike, M ;
Tsujimoto, I ;
Matsumura, Y ;
Sasaki, T ;
Hori, M ;
Otsu, K .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2004, 36 (06) :799-807