Jing Zhang, Jun Jiang, Bingqing Wang, Yue Wang, Yaoyao Qian, Jinmeng Suo, Yiming Li, Zhiyong Peng
The pathological mechanism of sepsis-associated acute kidney injury (SA-AKI) is complex and involves tubular epithelial cell (TEC) death and immune cell activation. However, the interaction between tubular cell death and macrophage-mediated inflammation remains unclear. In this study, we uncovered that TEC ferroptosis was activated in SA-AKI. Increased levels of ferroptotic markers, including ferroptosis-related proteins, lipid peroxidation, malondialdehyde (MDA), 4-hydroxynonenal (4-HNE), reactive oxygen species (ROS), and mitochondrial damage, were observed in the kidney tissue of cecum ligation and puncture (CLP) and Lipopolysaccharide (LPS)-induced SA-AKI mouse models, which were subsequently suppressed by Ferrostatin-1 (Fer-1)...
February 5, 2024: International Immunopharmacology