医学
乙酰化
串扰
氧化应激
心肌缺血
缺血
再灌注损伤
西妥因1
心脏病学
内科学
药理学
生物化学
下调和上调
基因
生物
物理
光学
作者
Qi Li,Zhuqing Li,Tingting Li,Chunlei Liu,Chengzhi Lu
标识
DOI:10.1016/j.ijcard.2022.03.019
摘要
We read with great interest the article by Xu et al. [ [1] Xu J.J. Cui J. Lin Q. et al. Protection of the enhanced Nrf2 deacetylation and its downstream transcriptional activity by SIRT1 in myocardial ischemia/reperfusion injury. Int. J. Cardiol. 2021; 342: 82-93 Google Scholar ], who demonstrated that SIRT1 protects cardiomyocytes from severe oxidative stress during myocardial ischemia/reperfusion injury (MI/RI) and such cardioprotective effects of SIRT1 are predominantly associated with the increased nuclear factor erythroid 2-related factor 2 (Nrf2) deacetylation and activity. This study highlighted the role of post-translational modification of proteins through changing the acetylation status of Nrf2 mediated by SIRT1 contributed to the modulation of oxidative stress and MI/RI treatment.
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