Redox Signaling in Cardiac Physiology and Pathology

被引:409
作者
Burgoyne, Joseph R. [2 ]
Mongue-Din, Heloise [1 ]
Eaton, Philip [2 ]
Shah, Ajay M. [1 ]
机构
[1] Kings Coll London, James Black Ctr, British Heart Fdn Ctr Excellence, Div Cardiovasc, London SE5 9NU, England
[2] St Thomas Hosp, Rayne Inst, London SE1 7EH, England
基金
英国惠康基金;
关键词
myocardial contractility; cardiac hypertrophy; NAD(P)H oxidase; oxidant signaling; MITOCHONDRIAL PERMEABILITY TRANSITION; MYOCARDIAL-ISCHEMIA-REPERFUSION; INDUCED CARDIOMYOCYTE HYPERTROPHY; NOX2-CONTAINING NADPH OXIDASE; HYPOXIA-INDUCIBLE FACTOR; HUMAN HEART-FAILURE; FACTOR-KAPPA-B; REACTIVE OXYGEN; ANGIOTENSIN-II; OXIDATIVE STRESS;
D O I
10.1161/CIRCRESAHA.111.255216
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Redox signaling refers to the specific and usually reversible oxidation/reduction modification of molecules involved in cellular signaling pathways. In the heart, redox signaling regulates several physiological processes (eg, excitation-contraction coupling) and is involved in a wide variety of pathophysiological and homoeostatic or stress response pathways. Reactive oxygen species involved in cardiac redox signaling may derive from many sources, but NADPH oxidases, as dedicated sources of signaling reactive oxygen species, seem to be especially important. An increasing number of specific posttranslational oxidative modifications involved in cardiac redox signaling are being defined, along with the reactive oxygen species sources that are involved. Here, we review current knowledge on the molecular targets of signaling reactive oxygen species in cardiac cells and their involvement in cardiac physiopathology. Advances in this field may allow the development of targeted therapeutic strategies for conditions such as heart failure as opposed to the general antioxidant approaches that have failed to date. (Circ Res. 2012;111:1091-1106.)
引用
收藏
页码:1091 / 1106
页数:16
相关论文
共 159 条
[1]   S-glutathiolation by peroxynitrite activates SERCA during arterial relaxation by nitric oxide [J].
Adachi, T ;
Weisbrod, RM ;
Pimentel, DR ;
Ying, J ;
Sharov, VS ;
Schöneich, C ;
Cohen, RA .
NATURE MEDICINE, 2004, 10 (11) :1200-1207
[2]   Role of Rac1 GTPase activation in atrial fibrillation [J].
Adam, Oliver ;
Frost, Gregg ;
Custodis, Florian ;
Sussman, Mark A. ;
Schaefers, Hans-Joachim ;
Boehm, Michael ;
Laufs, Ulrich .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2007, 50 (04) :359-367
[3]   Targeting an antioxidant to mitochondria decreases cardiac ischemia-reperfusion injury [J].
Adlam, VJ ;
Harrison, JC ;
Porteous, CM ;
James, AM ;
Smith, RAJ ;
Murphy, MP ;
Sammut, IA .
FASEB JOURNAL, 2005, 19 (09) :1088-1095
[4]   A redox-dependent pathway for regulating class IIHDACs and cardiac hypertrophy [J].
Ago, Tetsuro ;
Liu, Tong ;
Zhai, Peiyong ;
Chen, Wei ;
Li, Hong ;
Molkentin, Jeffery D. ;
Vatner, Stephen F. ;
Sadoshima, Junichi .
CELL, 2008, 133 (06) :978-993
[5]   Upregulation of Nox4 by Hypertrophic Stimuli Promotes Apoptosis and Mitochondrial Dysfunction in Cardiac Myocytes [J].
Ago, Tetsuro ;
Kuroda, Junya ;
Pain, Jayashree ;
Fu, Cexiong ;
Li, Hong ;
Sadoshima, Junichi .
CIRCULATION RESEARCH, 2010, 106 (07) :1253-U183
[6]   Reactive oxygen species in mechanical stress-induced cardiac hypertrophy [J].
Aikawa, R ;
Nagai, T ;
Tanaka, M ;
Zou, YZ ;
Ishihara, T ;
Takano, H ;
Hasegawa, H ;
Akazawa, H ;
Mizukami, M ;
Nagai, R ;
Komuro, I .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2001, 289 (04) :901-907
[7]   Redox-optimized ROS balance: A unifying hypothesis [J].
Aon, M. A. ;
Cortassa, S. ;
O'Rourke, B. .
BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS, 2010, 1797 (6-7) :865-877
[8]   Nicotinamide Adenine Dinucleotide Phosphate Oxidase in Experimental Liver Fibrosis: GKT137831 as a Novel Potential Therapeutic Agent [J].
Aoyama, Tomonori ;
Paik, Yong-Han ;
Watanabe, Sumio ;
Laleu, Benoit ;
Gaggini, Francesca ;
Fioraso-Cartier, Laetitia ;
Molango, Sophie ;
Heitz, Freddy ;
Merlot, Cedric ;
Szyndralewiez, Cedric ;
Page, Patrick ;
Brenner, David A. .
HEPATOLOGY, 2012, 56 (06) :2316-2327
[9]   Redox-mediated activation of latent transforming growth factor-beta 1 [J].
BarcellosHoff, MH ;
Dix, TA .
MOLECULAR ENDOCRINOLOGY, 1996, 10 (09) :1077-1083
[10]   The NOX family of ROS-generating NADPH oxidases: Physiology and pathophysiology [J].
Bedard, Karen ;
Krause, Karl-Heinz .
PHYSIOLOGICAL REVIEWS, 2007, 87 (01) :245-313