NADPH oxidase and heart failure

被引：52

作者：

Murdoch, CE ^{[1
]}

Grieve, DJ ^{[1
]}

Cave, AC ^{[1
]}

Looi, YH ^{[1
]}

Shah, AM ^{[1
]}

机构：

[1] Kings Coll London, Dept Cardiol, Div Cardiovasc, London SE5 9PJ, England

来源：

CURRENT OPINION IN PHARMACOLOGY | 2006年 / 6卷 / 02期

关键词：

D O I：

10.1016/j.coph.2005.10.008

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Reactive oxygen species play important roles in the pathophysiology of chronic heart failure secondary to chronic left ventricular hypertrophy or myocardial infarction. Reactive oxygen species influence several components of the phenotype of the failing heart, including contractile function, interstitial fibrosis, endothelial dysfunction and myocyte hypertrophy. Recent studies implicate the production of reactive oxygen species by a family of NADPH oxidases in these effects. NADPH oxidases are activated in an isoform-specific manner by many pathophysiological stimuli and exert distinct downstream effects. Understanding NADPH oxidase activation and regulation, and their downstream effectors, could help to develop novel therapeutic targets.

引用

页码：148 / 153

页数：6

共 35 条

[21] Oxidation of tetrahydrobiopterin leads to uncoupling of endothelial cell nitric oxide synthase in hypertension [J].

Landmesser, U ;

Dikalov, S ;

Price, SR ;

McCann, L ;

Fukai, T ;

Holland, SM ;

Mitch, WE ;

Harrison, DG .

JOURNAL OF CLINICAL INVESTIGATION, 2003, 111 (08) :1201-1209

[22] Activation of NADPH oxidase during progression of cardiac hypertrophy to failure [J].

Li, JM ;

Gall, NP ;

Grieve, DJ ;

Chen, MY ;

Shah, AM .

HYPERTENSION, 2002, 40 (04) :477-484

[23] Endothelial cell superoxide generation: regulation and relevance for cardiovascular pathophysiology [J].

Li, JM ;

Shah, AM .

AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, 2004, 287 (05) :R1014-R1030

[24]

Looi YH, 2005, CIRCULATION, V112, pU66

[25] Oxidative stress in the infarcted heart: role of de novo angiotensin II production [J].

Lu, L ;

Quinn, MT ;

Sun, Y .

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2004, 325 (03) :943-951

[26] Oxygen free radical release in human failing myocardium is associated with increased activity of Rac1-GTPase and represents a target for statin treatment [J].

Maack, C ;

Kartes, T ;

Kilter, H ;

Schäfers, HJ ;

Nickenig, G ;

Böhm, M ;

Laufs, U .

CIRCULATION, 2003, 108 (13) :1567-1574

[27] Impaired endothelial regulation of ventricular relaxation in cardiac hypertrophy - Role of reactive oxygen species and NADPH oxidase [J].

MacCarthy, PA ;

Grieve, DJ ;

Li, JM ;

Dunster, C ;

Kelly, FJ ;

Shah, AM .

CIRCULATION, 2001, 104 (24) :2967-2974

[28] Targeted deletion or pharmacological inhibition of MMP-2 prevents cardiac rupture after myocardial infarction in mice [J].

Matsumura, S ;

Iwanaga, S ;

Mochizuki, S ;

Okamoto, H ;

Ogawa, S ;

Okada, Y .

JOURNAL OF CLINICAL INVESTIGATION, 2005, 115 (03) :599-609

[29] Pressure overload-induced myocardial hypertrophy in mice does not require gp91phox [J].

Maytin, M ;

Siwik, DA ;

Ito, M ;

Xiao, L ;

Sawyer, DB ;

Liao, R ;

Colucci, WS .

CIRCULATION, 2004, 109 (09) :1168-1171

[30] Hyperglycemia activates JAK2 signaling pathway in human failing myocytes via angiotensin II-Mediated oxidative stress [J].

Modesti, A ;

Bertolozzi, L ;

Gamberi, T ;

Marchetta, M ;

Lumachi, C ;

Coppo, M ;

Moroni, F ;

Toscano, T ;

Lucchese, G ;

Gensini, GF ;

Modesti, PA .

DIABETES, 2005, 54 (02) :394-401

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