Thioredoxin in the cardiovascular system

被引：78
作者：
World, Cameron J.
Yamawaki, Hideyuki
Berk, Bradford C. [1 ]
机构：
[1] Univ Rochester, Dept Med, Inst Cardiovasc Res, Rochester, NY USA
[2] Natl Cardiovasc Ctr, Dept Epidemiol, Inst Res, Suita, Osaka 5658565, Japan
来源：
JOURNAL OF MOLECULAR MEDICINE-JMM | 2006年 / 84卷 / 12期
关键词：
antioxidants; cardiovascular diseases; endothelium; smooth muscle; signal transduction;
D O I：
10.1007/s00109-006-0109-6
中图分类号：
Q3 [遗传学];
学科分类号：
071007 ; 090102 ;
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 impairment of cell redox state alters multiple cell pathways, which may contribute to the pathogenesis of cardiovascular disorders including hypertension, atherosclerosis, and heart failure. In this manuscript, we review the essential roles that TRX plays by limiting oxidative stress directly via antioxidant effects and indirectly by protein-protein interactions with key signaling molecules such as thioredoxin interacting protein (TXNlP). TRX and its endogenous regulators may represent important future targets to develop clinical therapies for diseases associated with oxidative stress.
引用
收藏
页码：997 / 1003
页数：7
相关论文
共 59 条
[1]   Protection against reperfusion-induced arrhythmias by human thioredoxin [J].
Aota, M ;
Matsuda, K ;
Isowa, N ;
Wada, H ;
Yodoi, JJ ;
Ban, T .
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, 1996, 27 (05) :727-732
[2]  
Beckman JS, 1996, AM J PHYSIOL-CELL PH, V271, pC1424
[3]   The histone deacetylase inhibitor SAHA arrests cancer cell growth, up-regulates thioredoxin-binding protein-2, and down-regulates thioredoxin [J].
Butler, LM ;
Zhou, XB ;
Xu, WS ;
Scher, HI ;
Rifkind, RA ;
Marks, PA ;
Richon, VM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (18) :11700-11705
[4]  
CHAE HZ, 1994, J BIOL CHEM, V269, P27670
[5]   ISOLATION AND CHARACTERIZATION OF A NOVEL CDNA FROM HL-60 CELLS TREATED WITH 1,25-DIHYDROXYVITAMIN D-3 [J].
CHEN, KS ;
DELUCA, HF .
BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION, 1994, 1219 (01) :26-32
[6]   Oxidative stress and thioredoxin-interacting protein promote intravasation of melanoma cells [J].
Cheng, GC ;
Schulze, PC ;
Lee, RT ;
Sylvan, J ;
Zetter, BR ;
Huang, H .
EXPERIMENTAL CELL RESEARCH, 2004, 300 (02) :297-307
[7]   Two distinct mechanisms for loss of thioredoxin-binding protein-2 in oxidative stress-induced renal carcinogenesis [J].
Dutta, KK ;
Nishinaka, Y ;
Masutani, H ;
Akatsuka, S ;
Aung, TT ;
Shirase, T ;
Lee, WH ;
Yamada, Y ;
Hiai, H ;
Yodoi, JJ ;
Toyokuni, S .
LABORATORY INVESTIGATION, 2005, 85 (06) :798-807
[8]   Identification of novel differentially expressed genes by the effect of a high-fat n-6 diet in experimental breast cancer [J].
Escrich, E ;
Moral, R ;
Garcia, G ;
Costa, L ;
Sánchez, JA ;
Solanas, M .
MOLECULAR CARCINOGENESIS, 2004, 40 (02) :73-78
[9]   Thioredoxin reductase 1 is upregulated in atherosclerotic plaques:: Specific induction of the promoter in human macrophages by oxidized low-density lipoproteins [J].
Furman, C ;
Rundlöf, AK ;
Larigauderie, G ;
Jaye, M ;
Bricca, G ;
Copin, C ;
Kandoussi, AM ;
Fruchart, JC ;
Arnér, ESJ ;
Rouis, M .
FREE RADICAL BIOLOGY AND MEDICINE, 2004, 37 (01) :71-85
[10]   Redox regulatory and anti-apoptotic functions of thioredoxin depend on S-nitrosylation at cysteine 69 [J].
Haendeler, J ;
Hoffmann, J ;
Tischler, V ;
Berk, BC ;
Zeiher, AM ;
Dimmeler, S .
NATURE CELL BIOLOGY, 2002, 4 (10) :743-749
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