NADPH oxidase CYBA polymorphisms, oxidative stress and cardiovascular diseases

被引：75

作者：

Jose, Gorka San ^{[1
]}

Fortuno, Ana ^{[1
]}

Beloqui, Oscar ^{[2
]}

Diez, Javier ^{[1
,3
]}

Zalba, Guillermo ^{[1
]}

机构：

[1] Univ Navarra, Sch Med, Ctr Appl Med Res, Div Cardiovasc Sci, E-31080 Pamplona, Spain

[2] Univ Navarra, Sch Med, Dept Internal Med, E-31080 Pamplona, Spain

[3] Univ Navarra, Sch Med, Univ Clin, Dept Cardiol & Cardiovasc Surg, E-31080 Pamplona, Spain

来源：

CLINICAL SCIENCE | 2008年 / 114卷 / 3-4期

关键词：

cardiovascular disease; NADPH oxidase; oxidative stress; p22(phox) subunit; reactive oxygen species (ROS); superoxide anion;

D O I：

10.1042/CS20070130

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：

Oxidative stress plays a key role in the pathophysiology of several major cardiovascular diseases, including atherosclerosis, hypertension, heart failure, stroke and diabetes. ROS (reactive oxygen species) affect multiple tissues either directly or through NO depletion. ROS induce cardiovascular dysfunction by modulating cell contraction/dilation, migration, growth/apoptosis and extracellular matrix protein turnover, which contribute to vascular and cardiac remodelling. Of the several sources of ROS within the cardiovascular system, a family of multisubunit NADPH oxidases appears to be a predominant contributor of superoxide anion. Recent findings suggest a significant role of the genetic background in NADPH oxidase regulation. Common genetic polymorphisms within the promoter and exonic sequences of CYBA, the gene that encodes the P22(phox) subunit of NADPH oxidase, have been characterized in the context of cardiovascular diseases. This review aims to present the current state of research into these polymorphisms in their relationship to cardiovascular diseases.

引用

页码：173 / 182

页数：10

共 106 条

[1]

Ardanaz N, 2006, EXP BIOL MED, V231, P237

[2]

Beckman JS, 1996, AM J PHYSIOL-CELL PH, V271, pC1424

[3] The NOX family of ROS-generating NADPH oxidases: Physiology and pathophysiology [J].

Bedard, Karen ;

Krause, Karl-Heinz .

PHYSIOLOGICAL REVIEWS, 2007, 87 (01) :245-313

[4] NADPH oxidases: not just for leukocytes anymore! [J].

Bokoch, GM ;

Knaus, UG .

TRENDS IN BIOCHEMICAL SCIENCES, 2003, 28 (09) :502-508

[5] Vascular NADPH oxidases: molecular mechanisms of activation [J].

Brandes, RP ;

Kreuzer, J .

CARDIOVASCULAR RESEARCH, 2005, 65 (01) :16-27

[6] A variant of p22phox, involved in generation of reactive oxygen species in the vessel wall, is associated with progression of coronary atherosclerosis [J].

Cahilly, C ;

Ballantyne, CM ;

Lim, DS ;

Gotto, A ;

Marian, AJ .

CIRCULATION RESEARCH, 2000, 86 (04) :391-395

[7]

Cai H, 1999, EUR J CLIN INVEST, V29, P744

[8] Endothelial dysfunction in cardiovascular diseases - The role of oxidant stress [J].

Cai, H ;

Harrison, DG .

CIRCULATION RESEARCH, 2000, 87 (10) :840-844

[9] NADPH oxidase-derived reactive oxygen species in cardiac pathophysiology [J].

Cave, A ;

Grieve, D ;

Johar, S ;

Zhang, M ;

Shah, AM .

PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES, 2005, 360 (1464) :2327-2334

[10] Targeting reactive oxygen species in hypertension [J].

Cifuentes, ME ;

Pagano, PJ .

CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION, 2006, 15 (02) :179-186

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