文献类型：期刊文献

英文题名：Prospect of thioredoxin as a possibly effective tool to combat OSAHS

作者：Pan, Ye[1];Lu, You[1];Zhou, Jie-dong[1];Wang, Cui-xue[1];Wang, Jin-quan[1];Fukunaga, Atsushi[2];Yodoi, Junji[3];Tian, Hai[1,4]

机构：[1]Shaoxing Univ, Dept Basic Med, Coll Med, Shaoxing, Peoples R China;[2]Kobe Univ, Div Dermatol, Dept Internal Related, Grad Sch Med, Kobe, Hyogo, Japan;[3]Kyoto Univ, Inst Virus Res, Dept Biol Response, Lab Infect & Prevent, Kyoto, Japan;[4]Jiaozhimei Biotechnol CO Ltd, Shaoxing, Peoples R China

年份：0

外文期刊名：SLEEP AND BREATHING

收录：SCI-EXPANDED(收录号：WOS:000805538900001)、、Scopus(收录号：2-s2.0-85130993793)、WOS

语种：英文

外文关键词：Thioredoxin; OSAHS; Molecular mechanisms; Prospect

外文摘要：Purpose Obstructive sleep apnea-hypopnea syndrome (OSAHS) is characterized by recurrent upper airway disturbances during sleep leading to episodes of hypopnea or apnea, followed by hypoxemia and subsequent reoxygenation. It is believed that this reoxygenation/reperfusion stage leads to oxidative stress, which then leads to inflammation and cardiovascular diseases. The treatments of patient with OSAHS include surgical and non-surgical therapies with various side effects and common complaints. Therefore, it is important to develop a new, safe, and effective therapeutic treatment. As a small-molecule multifunctional protein, thioredoxin (TRX) has antioxidant and redox regulatory functions at the active site Cys-Gly-Pro. TRX prevents inflammation by suppressing the production of pro-inflammatory cytokines rather than suppressing the immune response. Methods We review the papers on the pathophysiological process of OSAHS and the antioxidative and anti-inflammatory effects of TRX. Results TRX may play a role in OSAHS by scavenging ROS, blocking the production of inflammatory cytokines, inhibiting the migration and activation of neutrophils, and controlling the activation of ROS-dependent inflammatory signals by regulating the redox state of intracellular target particles. Furthermore, TRX regulates the synthesis, stability, and activity of hypoxia-inducible factor 1 (HIF-1). TRX also has an inhibitory effect on endoplasmic reticulum- and mitochondria-induced apoptosis by regulating the expression of BAX, BCL2, p53, and ASK1. Conclusion Understanding the function of TRX may be useful for the treatment of OSAHS.