Journal
JOURNAL OF CELLULAR PHYSIOLOGY
Volume 236, Issue 2, Pages 931-945Publisher
WILEY
DOI: 10.1002/jcp.29903
Keywords
AKI; GPX4; irisin; renal I; R; ROS
Categories
Funding
- Xi'an Jiaotong University
- Ministry of Education Innovation Team Development Program of China [IRT16R57]
- National Natural Science Foundation of China [81701960, 81770491]
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Irisin attenuates I/R-induced AKI by upregulating GPX4, improving renal injury, and inhibiting inflammatory response and oxidative stress.
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 mu g/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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