| Literature DB >> 33310138 |
Yunxia Liu1, Meina Li2, Xiaoyu Du1, Zhehao Huang3, Nanhu Quan4.
Abstract
Physiological reactive oxygen species (ROS) play an important role in cellular signal transduction. However, excessive ROS is an important pathological mechanism in most cardiovascular diseases (CVDs), such as myocardial aging, cardiomyopathy, ischemia/reperfusion injury (e.g., myocardial infarction) and heart failure. Programmed cell death, hypertrophy and fibrosis may be due to oxidative stress. Sestrin 2 (Sesn2), a stress-inducible protein associated with various stress conditions, is a potential antioxidant. Sesn2 can suppress the process of heart damage caused by oxidative stress, promote cell survival and play a key role in a variety of CVDs. This review discusses the effect of Sesn2 on the redox signal, mainly via participation in the signaling pathway of nuclear factor erythroid 2-related factor 2, activation of adenosine monophosphate-activated protein kinase and inhibition of mammalian target of rapamycin complex 1. It also discusses the effect of Sesn2's antioxidant activity on different CVDs. We speculate that Sesn2 plays an important role in CVDs by stimulating the process of antioxidation and promoting the adaptation of cells to stress conditions and/or the environment, opening a new avenue for related therapeutic strategies.Entities:
Keywords: Cardiovascular diseases; Oxidative stress; Sestrin 2
Year: 2020 PMID: 33310138 DOI: 10.1016/j.freeradbiomed.2020.11.015
Source DB: PubMed Journal: Free Radic Biol Med ISSN: 0891-5849 Impact factor: 7.376