Thioredoxin - A key regulator of cardiovascular homeostasis

被引：185

作者：

Yamawaki, H

Haendeler, J

Berk, BC

机构：

[1] Univ Rochester, Cardiovasc Res Ctr, Rochester, NY 14642 USA

[2] Univ Frankfurt, Dept Mol Cardiol, D-6000 Frankfurt, Germany

来源：

CIRCULATION RESEARCH | 2003年 / 93卷 / 11期

关键词：

antioxidants; cardiovascular diseases; endothelium; smooth muscle; signal transduction;

D O I：

10.1161/01.RES.0000102869.39150.23

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The thioredoxin (TRX) system (TRX, TRX reductase, and NADPH) is a ubiquitous thiol oxidoreductase system that regulates cellular reduction/ oxidation ( redox) status. The oxidation mechanism for disease pathogenesis states that an imbalance in cell redox state alters function of multiple cell pathways. In this study, we review the essential role for TRX to limit oxidative stress directly via antioxidant effects and indirectly by protein-protein interaction with key signaling molecules, such as apoptosis signal-regulating kinase 1. We propose that TRX and its endogenous regulators are important future targets to develop clinical therapies for cardiovascular disorders associated with oxidative stress.

引用

收藏

页码：1029 / 1033

页数：5

相关论文

共 50 条

[41] Thioredoxin-2 (TRX-2) is an essential gene regulating mitochondria-dependent apoptosis [J].

Tanaka, T ;

Hosoi, F ;

Yamaguchi-Iwai, Y ;

Nakamura, H ;

Masutani, H ;

Ueda, S ;

Nishiyama, A ;

Takeda, S ;

Wada, H ;

Spyrou, G ;

Yodoi, J .

EMBO JOURNAL, 2002, 21 (07) :1695-1703

[42] Thioredoxin redox signaling in the ischemic heart: an insight with transgenic mice overexpressing Trx1 [J].

Turoczi, T ;

Chang, VWH ;

Engelman, RM ;

Maulik, N ;

Ho, YS ;

Das, DK .

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2003, 35 (06) :695-704

[43] Vitamin D3-up-regulated protein-1 is a stress-responsive gene that regulates cardiomyocyte viability through interaction with thioredoxin [J].

Wang, YL ;

De Keulenaer, GW ;

Lee, RT .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (29) :26496-26500

[44] Redox potential of human thioredoxin 1 and identification of a second dithiol/disulfide motif [J].

Watson, WH ;

Pohl, J ;

Montfort, WR ;

Stuchlik, O ;

Reed, MS ;

Powis, G ;

Jones, DP .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (35) :33408-33415

[45] Crystal structures of reduced, oxidized, and mutated human thioredoxins: Evidence for a regulatory homodimer [J].

Weichsel, A ;

Gasdaska, JR ;

Powis, G ;

Montfort, WR .

STRUCTURE, 1996, 4 (06) :735-751

[46] Thioredoxin facilitates the induction of heme oxygenase-1 in response to inflammatory mediators [J].

Wiesel, P ;

Foster, LC ;

Pellacani, A ;

Layne, MD ;

Hsieh, CM ;

Huggins, GS ;

Strauss, P ;

Yet, SF ;

Perrella, MA .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (32) :24840-24846

[47] REDOX ACTIVATION OF FOS JUN DNA-BINDING ACTIVITY IS MEDIATED BY A DNA-REPAIR ENZYME [J].

XANTHOUDAKIS, S ;

MIAO, G ;

WANG, F ;

PAN, YCE ;

CURRAN, T .

EMBO JOURNAL, 1992, 11 (09) :3323-3335

[48] Chronic physiological shear stress inhibits tumor necrosis factor-induced proinflammatory responses in rabbit aorta perfused ex vivo [J].

Yamawaki, H ;

Lehoux, S ;

Berk, BC .

CIRCULATION, 2003, 108 (13) :1619-1625

[49]

Yoshida S, 1999, J IMMUNOL, V163, P351

[50] Thioredoxin overexpression prevents NO-induced reduction of NO synthase activity in lung endothelial cells [J].

Zhang, JL ;

Li, YD ;

Patel, JM ;

Block, ER .

AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 1998, 275 (02) :L288-L293

← 1 2 3 4 5 →