NO/redox disequilibrium in the failing heart and cardiovascular system

被引:276
作者
Hare, JM
Stamler, JS
机构
[1] Duke Univ, Sch Med, Howard Hughes Med Inst, Dept Med, Durham, NC USA
[2] Duke Univ, Sch Med, Howard Hughes Med Inst, Dept Biochem, Durham, NC USA
关键词
D O I
10.1172/JCI200524459
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
There is growing evidence that the altered production and/or spatiotemporal distribution of reactive oxygen and nitrogen species creates oxidative and/or nitrosative stresses in the failing heart and vascular tree, which contribute to the abnormal cardiac and vascular phenotypes that characterize the failing cardiovascular system. These derangements at the integrated system level can be interpreted at the cellular and molecular levels in terms of adverse effects on signaling elements in the heart, vasculature, and blood that subserve cardiac and vascular homeostasis.
引用
收藏
页码:509 / 517
页数:9
相关论文
共 100 条
[1]  
ABUSOUD H, 2005, J BIOL CHEM, V271, P32515
[2]   Production of superoxide from hemoglobin-bound oxygen under hypoxic conditions [J].
Balagopalakrishna, C ;
Manoharan, PT ;
Abugo, OO ;
Rifkind, JM .
BIOCHEMISTRY, 1996, 35 (20) :6393-6398
[3]   NITRIC OXIDE-DEPENDENT PARASYMPATHETIC SIGNALING IS DUE TO ACTIVATION OF CONSTITUTIVE ENDOTHELIAL (TYPE-III) NITRIC-OXIDE SYNTHASE IN CARDIAC MYOCYTES [J].
BALLIGAND, JL ;
KOBZIK, L ;
HAN, XQ ;
KAYE, DM ;
BELHASSEN, L ;
OHARA, DS ;
KELLY, RA ;
SMITH, TW ;
MICHEL, T .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (24) :14582-14586
[4]   Nitric oxide regulates the heart by spatial confinement of nitric oxide synthase isoforms [J].
Barouch, LA ;
Harrison, RW ;
Skaf, MW ;
Rosas, GO ;
Cappola, TP ;
Kobeissi, ZA ;
Hobai, IA ;
Lemmon, CA ;
Burnett, AL ;
O'Rourke, B ;
Rodriguez, ER ;
Huang, PL ;
Lima, JAC ;
Berkowitz, DE ;
Hare, JM .
NATURE, 2002, 416 (6878) :337-340
[5]   Combined loss of neuronal and endothelial nitric oxide synthase causes premature mortality and age-related hypertrophic cardiac remodeling in mice [J].
Barouch, LA ;
Cappola, TP ;
Harrison, RW ;
Crone, JK ;
Rodriguez, ER ;
Burnett, AL ;
Hare, JM .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2003, 35 (06) :637-644
[6]   Xanthine oxicloreductase and cardiovascular disease: molecular mechanisms and pathophysiological implications [J].
Berry, CE ;
Hare, JM .
JOURNAL OF PHYSIOLOGY-LONDON, 2004, 555 (03) :589-606
[7]   NITRIC-OXIDE DIRECTLY ACTIVATES CALCIUM-DEPENDENT POTASSIUM CHANNELS IN VASCULAR SMOOTH-MUSCLE [J].
BOLOTINA, VM ;
NAJIBI, S ;
PALACINO, JJ ;
PAGANO, PJ ;
COHEN, RA .
NATURE, 1994, 368 (6474) :850-853
[8]   Interaction of nitric oxide synthase with the postsynaptic density protein PSD-95 and alpha 1-syntrophin mediated by PDZ domains [J].
Brenman, JE ;
Chao, DS ;
Gee, SH ;
McGee, AW ;
Craven, SE ;
Santillano, DR ;
Wu, ZQ ;
Huang, F ;
Xia, HH ;
Peters, MF ;
Froehner, SC ;
Bredt, DS .
CELL, 1996, 84 (05) :757-767
[9]   Allopurinol improves myocardial efficiency in patients with idiopathic dilated cardiomyopathy [J].
Cappola, TP ;
Kass, DA ;
Nelson, GS ;
Berger, RD ;
Rosas, GO ;
Kobeissi, ZA ;
Marbán, E ;
Hare, JM .
CIRCULATION, 2001, 104 (20) :2407-2411
[10]   Deficiency of different nitric oxide synthase isoforms activates divergent transcriptional programs in cardiac hypertrophy [J].
Cappola, TP ;
Cope, L ;
Cernetich, A ;
Barouch, LA ;
Minhas, K ;
Irizarry, RA ;
Parmigiani, G ;
Durrani, S ;
Lavoie, T ;
Hoffman, EP ;
Ye, SQ ;
Garcia, JGN ;
Hare, JM .
PHYSIOLOGICAL GENOMICS, 2003, 14 (01) :25-34