GPX4
急性肾损伤
氧化应激
缺血
下调和上调
活性氧
医学
内分泌学
肾
再灌注损伤
肾功能
谷胱甘肽过氧化物酶
内科学
化学
生物化学
超氧化物歧化酶
基因
作者
Jia Zhang,Jianbin Bi,Yifan Ren,Zhaoqing Du,Li Teng,Tao Wang,Lin Zhang,Mengzhou Wang,Shasha Wei,Yi Lv,Rongqian Wu
摘要
Abstract Ischemia reperfusion (I/R)‐induced acute kidney injury (AKI) is a common and serious condition. Irisin, an exercise‐induced hormone, improves mitochondrial function and reduces reactive oxygen species (ROS) production. Glutathione peroxidase 4 (GPX4) is a key regulator of ferroptosis and its inactivation aggravates renal I/R injury by inducing ROS production. However, the effect of irisin on GPX4 and I/R‐induced AKI is still unknown. To study this, male adult mice were subjected to renal I/R by occluding bilateral renal hilum for 30 min, which was followed by 24 hr reperfusion. Our results showed serum irisin levels were decreased in renal I/R mice. Irisin (250 μg/kg) treatment alleviated renal injury, downregulated inflammatory response, improved mitochondrial function, and reduced ER stress and oxidative stress after renal I/R, which were associated with upregulation of GPX4. Treated with RSL3 (a GPX4 inhibitor) abolished irisin's protective effect. Thus, irisin attenuates I/R‐induced AKI through upregulating GPX4.
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