Dephosphorylation of AMP-activated kinase exacerbates ischemia/reperfusion-induced acute kidney injury via mitochondrial dysfunction.

Kidney tubular epithelial cells are high energy-consuming epithelial cells that depend mainly on fatty acid oxidation for an energy supply. AMP-activated protein kinase (AMPK) is a key regulator of energy production in most cells, but the function of AMPK in tubular epithelial cells in acute kidney disease is unclear. Here, we found a rapid decrease in Thr172-AMPK α phosphorylation after ischemia/reperfusion in both in vivo and in vitro models. Mice with kidney tubular epithelial cell-specific AMPKα deletion exhibited exacerbated kidney impairment and apoptosis of tubular epithelial cells after ischemia/reperfusion.

Source: Kidney International - November 10, 2021 Category: Urology & Nephrology Authors: Haijian Ma, Xiaozhen Guo, Shichao Cui, Yongmei Wu, Yangming Zhang, Xiaoyan Shen, Cen Xie, Jingya Li Tags: basic research Source Type: research