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氧化应激是肾脏纤维化形成的关键因素之一,它的持续存在可刺激多种细胞因子、激活多条信号通路,贯穿肾脏纤维化发生、发展的始终。丝裂原活化蛋白激酶(MAPK)是细胞内介导胞外刺激的重要信号通路,是细胞促增殖和传递应激信号的关键激酶。其中,p38 MAPK是MAPK家族成员之一,在肿瘤、应激反应、炎症、缺血-再灌注损伤及免疫调控等领域发挥着重要作用,可以通过调节转化生长因子β1、核因子-κB及p53等因子的表达,从而影响肾间质纤维化的进程。本文主要就p38 MAPK信号通路在氧化应激诱导肾间质纤维化的研究新进展进行综述。
Oxidative stress is one of the key factors in the formation of renal fibrosis. Its persistence can stimulate a variety of cytokines, activate multiple signaling pathways, and throughout the development and progression of renal fibrosis. Mitogen-activated protein kinase (MAPK) is an important intracellular signal pathways that mediate extracellular stimuli and is a key kinase that stimulates cell proliferation and transmits stress signals. Among them, p38 MAPK, a member of the MAPK family, plays an important role in tumor, stress response, inflammation, ischemia-reperfusion injury and immune regulation, and can regulate the expression of transforming growth factor β1, nuclear factor-κB and p53 And other factors, thus affecting the process of renal interstitial fibrosis. This review summarizes the recent advances in the study of p38 MAPK signaling pathway in oxidative stress-induced renal interstitial fibrosis.