期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 22, 期 21, 页码 -出版社
MDPI
DOI: 10.3390/ijms222111411
关键词
antioxidant response element; Kelch-like ECH-associated protein 1; nuclear factor E2-related factor 2; nutritional regulation; ulcerative colitis
资金
- National Natural Science Foundation of China [32102587, 31930106, 31829004]
- National Ten-thousand Talents Program of China [23070201, 1041-00109019]
- 111 Project [B16044]
The Nrf2/ARE pathway plays a critical role in protecting against cellular stress and inflammation in diseases like ulcerative colitis. Both Keap1-dependent and Keap1-independent cascades have been proposed to positively affect the activation of this pathway. Nutritional compounds have the potential to modulate the activation of Nrf2/ARE pathway and may be used for therapeutic applications in UC.
Ulcerative colitis (UC), which affects millions of people worldwide, is characterized by extensive colonic injury involving mucosal and submucosal layers of the colon. Nuclear factor E2-related factor 2 (Nrf2) plays a critical role in cellular protection against oxidant-induced stress. Antioxidant response element (ARE) is the binding site recognized by Nrf2 and leads to the expression of phase II detoxifying enzymes and antioxidant proteins. The Nrf2/ARE system is a key factor for preventing and resolving tissue injury and inflammation in disease conditions such as UC. Researchers have proposed that both Keap1-dependent and Keap1-independent cascades contribute positive effects on activation of the Nrf2/ARE pathway. In this review, we summarize the present knowledge on mechanisms controlling the activation process. We will further review nutritional compounds that can modulate activation of the Nrf2/ARE pathway and may be used as potential therapeutic application of UC. These comprehensive data will help us to better understand the Nrf2/ARE signaling pathway and promote its effective application in response to common diseases induced by oxidative stress and inflammation.
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