期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 109, 期 -, 页码 125-131出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2016.12.020
关键词
Thioredoxin; Disulfide; Anti-oxidant; Ischemia/reperfusion
资金
- U.S. Public Health Service [HL67724, HL91469, HL102738, HL112330, AG23039]
- Leducq Foundation Transatlantic Network of Excellence
- American Heart Association, Founders Affiliate [14PRE20480412]
Myocardial ischemia/reperfusion and heart failure are the major cardiac conditions in which an imbalance between oxidative stress and anti-oxidant mechanisms is observed. The myocardium has endogenous reducing mechanisms, including the thioredoxin (Trx) and glutathione systems, that act to scavenge reactive oxygen species (ROS) and reduce oxidized proteins. The Trx system consists of Trx, Trx reductase (TrxR), and an electron donor, NADPH, where Trx is maintained in a reduced state in the presence of TrxR and NADPH. Trx1, a major isoform of Trx, is abundantly expressed in the heart and exerts its oxidoreductase activity through conserved Cys32 and Cys35, reducing oxidized proteins through thiol disulfide exchange reactions. In this review, we will focus on molecular targets of Trx1 in the heart, including transcription factors, microRNAs, histone deactylases, and protein kinases. We will then discuss how Trx1 regulates the functions of its targets, thereby affecting the extent of myocardial injury caused by myocardial ischemia/reperfusion and the progression of heart failure.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据