Redox mechanisms in blood vessels

被引:271
作者
Mueller, CFH
Laude, K
McNally, JS
Harrison, DG
机构
[1] Emory Univ, Div Cardiol, Dept Med, Atlanta, GA 30322 USA
[2] Atlanta Vet Adm Hosp, Atlanta, GA USA
关键词
NADPH oxidase; superoxide; nitric oxide synthase; xanthine oxidase; mitochondria;
D O I
10.1161/01.ATV.0000149143.04821.eb
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Reactive oxygen species have been implicated in the pathogenesis of virtually every stage of vascular lesion formation, hypertension, and other vascular diseases. We are currently gaining insight into important sources of reactive oxygen species in the vessel wall, including the NADPH oxidases, xanthine oxidase, uncoupled nitric oxide synthase, and mitochondrial sources. Although various reactive oxygen species have pathological roles, some serve as important signaling molecules that modulate vascular tone, growth, and remodeling. In the next several months, a series of articles in Arteriosclerosis, Thrombosis, and Vascular Biology attempt to further elucidate how reactive oxygen species are produced by vascular cells and the roles of these in vascular homeostasis. This series promises to provide a valuable update on a wide variety of issues related to the biochemistry, molecular biology, and physiology of these important and fascinating molecules.
引用
收藏
页码:274 / 278
页数:5
相关论文
共 64 条
[1]  
AFANAS EIB, 1989, SUPEROXIDE ION CHEM
[2]   Nox4 as the major catalytic component of an endothelial NAD(P)H oxidase [J].
Ago, T ;
Kitazono, T ;
Ooboshi, H ;
Iyama, T ;
Han, YH ;
Takada, J ;
Wakisaka, M ;
Ibayashi, S ;
Utsumi, H ;
Iida, M .
CIRCULATION, 2004, 109 (02) :227-233
[3]  
Albertini R., 2002, Current Molecular Medicine (Hilversum), V2, P579, DOI 10.2174/1566524023362177
[4]   Mitochondrial requirement for endothelial responses to cyclic strain: implications for mechanotransduction [J].
Ali, MH ;
Pearlstein, DP ;
Mathieu, CE ;
Schumacker, PT .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 2004, 287 (03) :L486-L496
[5]   Tetrahydrobiopterin-dependent preservation of nitric oxide-mediated endothelial function in diabetes by targeted transgenic GTP-cyclohydrolase I overexpression [J].
Alp, NJ ;
Mussa, S ;
Khoo, J ;
Cai, SJ ;
Guzik, T ;
Jefferson, A ;
Goh, N ;
Rockett, KA ;
Channon, KM .
JOURNAL OF CLINICAL INVESTIGATION, 2003, 112 (05) :725-735
[6]   Direct interaction of the novel nox proteins with p22phox is required for the formation of a functionally active NADPH oxidase [J].
Ambasta, RK ;
Kumar, P ;
Griendling, KK ;
Schmidt, HHHW ;
Busse, R ;
Brandes, RP .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (44) :45935-45941
[7]   Hydrogen peroxide- and peroxynitrite-induced mitochondrial DNA damage and dysfunction in vascular endothelial and smooth muscle cells [J].
Ballinger, SW ;
Patterson, C ;
Yan, CN ;
Doan, R ;
Burow, DL ;
Young, CG ;
Yakes, FM ;
Van Houten, B ;
Ballinger, CA ;
Freeman, BA ;
Runge, MS .
CIRCULATION RESEARCH, 2000, 86 (09) :960-966
[8]   Two novel proteins activate superoxide generation by the NADPH oxidase NOX1 [J].
Bánfi, B ;
Clark, RA ;
Steger, K ;
Krause, KH .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (06) :3510-3513
[9]   Xanthine oxidase inhibition with oxypurinol improves endothelial vasodilator function in hypercholesterolemic but not in hypertensive patients [J].
Cardillo, C ;
Kilcoyne, CM ;
Cannon, RO ;
Quyyumi, AA ;
Panza, JA .
HYPERTENSION, 1997, 30 (01) :57-63
[10]   Redox regulation of protein tyrosine phosphatases by hydrogen peroxide: Detecting sulfenic acid intermediates and examining reversible inactivation [J].
Denu, JM ;
Tanner, KG .
PROTEIN SENSORS AND REACTIVE OXYGEN SPECIES, PT B, THIOL ENZYMES AND PROTEINS, 2002, 348 :297-305