心肌保护
KEAP1型
再灌注损伤
自噬
调节器
缺血
医学
氧化应激
缺血预处理
药理学
心脏病学
转录因子
化学
内科学
生物化学
细胞凋亡
基因
作者
Yiming Shen,Xiaojuan Liu,Jiahai Shi,Wu Xiang
标识
DOI:10.1016/j.ijbiomac.2018.11.190
摘要
The morbidity rate of myocardial ischemia and reperfusion has increased in modern society, and oxidative stress plays a critical role in the pathological process. Nuclear factor E2-associated factor 2 (Nrf2) is considered a pivotal regulator for maintaining the redox balance and is involved in the initiation of the transcriptional expression of downstream antioxidant enzymes. Moreover, Nrf2 also can be regulated in various ways. Nrf2/Keap1/ARE is one of the essential signaling pathways that can attenuate myocardial infarct size and preserve cardiac function after myocardial ischemia and reperfusion injury (MIRI). Nrf2 activation provides cardioprotection via the coordinated up-regulation of antioxidant, anti-inflammatory, and autophagy mechanisms. Numerous studies have shown that ischemic preconditioning and ischemic post-conditioning have a clear protective effect on MIRI, and the potential role of the Nrf2 signaling pathway in cardioprotection may be worth discussing. This review will summarize the current knowledge on the regulation of and involvement of Nrf2 in MIRI.
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