NADPH oxidases: key modulators in aging and age-related cardiovascular diseases?

被引：129

作者：

Sahoo, Sanghamitra ^{[1
]}

Meijles, Daniel N. ^{[1
]}

Pagano, Patrick J. ^{[1
]}

机构：

[1] Univ Pittsburgh, Vasc Med Inst, Dept Pharmacol & Chem Biol, Pittsburgh, PA 15261 USA

来源：

CLINICAL SCIENCE | 2016年 / 130卷 / 05期

基金：

美国国家卫生研究院;

关键词：

aging; cardiovascular diseases; reduced nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase; reduced nicotinamide-adenine dinucleotide phosphate oxidase therapeutics (Nox therapeutics); GROWTH-FACTOR-I; SMOOTH-MUSCLE-CELLS; VASCULAR OXIDATIVE STRESS; PULMONARY ARTERIAL-HYPERTENSION; NOX FAMILY PROTEINS; LIFE-SPAN; REACTIVE OXYGEN; ATRIAL-FIBRILLATION; NAD(P)H OXIDASE; SUPEROXIDE-PRODUCTION;

D O I：

10.1042/CS20150087

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：

Reactive oxygen species (ROS) and oxidative stress have long been linked to aging and diseases prominent in the elderly such as hypertension, atherosclerosis, diabetes and atrial fibrillation (AF). NADPH oxidases (Nox) are a major source of ROS in the vasculature and are key players in mediating redox signalling under physiological and pathophysiological conditions. In this review, we focus on the Nox-mediated ROS signalling pathways involved in the regulation of 'longevity genes' and recapitulate their role in age-associated vascular changes and in the development of age-related cardiovascular diseases (CVDs). This review is predicated on burgeoning knowledge that Nox-derived ROS propagate tightly regulated yet varied signalling pathways, which, at the cellular level, may lead to diminished repair, the aging process and predisposition to CVDs. In addition, we briefly describe emerging Nox therapies and their potential in improving the health of the elderly population.

引用

页码：317 / 335

页数：19

共 271 条

[31] Atrial fibrosis: Mechanisms and clinical relevance in atrial fibrillation [J].

Burstein, Brett ;

Nattel, Stanley .

JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2008, 51 (08) :802-809

[32] Redox state of tumor suppressor p53 regulates its sequence-specific DNA binding in DNA-damaged cells by cysteine 277 [J].

Buzek, J ;

Latonen, L ;

Kurki, S ;

Peltonen, K ;

Laiho, M .

NUCLEIC ACIDS RESEARCH, 2002, 30 (11) :2340-2348

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

Cai, H ;

Harrison, DG .

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

[34] The vascular NAD(P)H oxidases as therapeutic targets cardiovascular diseases [J].

Cai, H ;

Griendling, KK ;

Harrison, DG .

TRENDS IN PHARMACOLOGICAL SCIENCES, 2003, 24 (09) :471-478

[35] AGE-receptor-1 counteracts cellular oxidant stress induced by AGEs via negative regulation of p66shc-dependent FKHRL1 phosphorylation [J].

Cai, Weijing ;

He, John Cijiang ;

Zhu, Li ;

Chen, Xue ;

Striker, Gary E. ;

Vlassara, Helen .

AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 2008, 294 (01) :C145-C152

[36] Atrial myocardial nox2 containing NADPH oxidase activity contribution to oxidative stress in mitral regurgitation: potential mechanism for atrial remodeling [J].

Chang, Jen-Ping ;

Chen, Mien-Cheng ;

Liu, Wen-Hao ;

Yang, Cheng-Hsu ;

Chen, Chien-Jen ;

Chen, Yung-Lung ;

Pan, Kuo-Li ;

Tsai, Tzu-Hsien ;

Chang, Hsueh-Wen .

CARDIOVASCULAR PATHOLOGY, 2011, 20 (02) :99-106

[37] Upregulation of p67phox and gp91phox in aortas from angiotensin II-infused mice [J].

Cifuentes, ME ;

Rey, FE ;

Carretero, OA ;

Pagano, PJ .

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2000, 279 (05) :H2234-H2240

[38] The Quest for Selective Nox Inhibitors and Therapeutics: Challenges, Triumphs and Pitfalls [J].

Cifuentes-Pagano, Eugenia ;

Meijles, Daniel N. ;

Pagano, Patrick J. .

ANTIOXIDANTS & REDOX SIGNALING, 2014, 20 (17) :2741-2754

[39] Bridged tetrahydroisoquinolines as selective NADPH oxidase 2 (Nox2) inhibitors [J].

Cifuentes-Pagano, Eugenia ;

Saha, Jaideep ;

Csanyi, Gabor ;

Al Ghouleh, Imad ;

Sahoo, Sanghamitra ;

Rodriguez, Andres ;

Wipf, Peter ;

Pagano, Patrick J. ;

Skoda, Erin M. .

MEDCHEMCOMM, 2013, 4 (07) :1085-1092

[40] Reactive oxygen species as mediators of cellular senescence [J].

Colavitti, R ;

Finkel, T .

IUBMB LIFE, 2005, 57 (4-5) :277-281

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