Mitochondrial GPX4 acetylation is involved in cadmium-induced renal cell ferroptosis

• DOI: 10.1016/j.redox.2024.103179
• Publication Date: 2024-05-08T02:24:22Z
• Authors: Yue-Yue Guo; Nan-Nan Liang; Xiao-Yi Zhang; Ya-Hui Ren; Wen-Zheng Wu; Zhi-Bing Liu; Yi-Zhang He; Yi-Hao Zhang; Yi-Chao Huang; Tao Zhang; De-Xiang Xu; Shen Xu
• Keywords: GPX4; Cadmium poisoning

Increasing evidences demonstrate that environmental stressors are important inducers of acute kidney injury (AKI). This study aimed to investigate the impact exposure Cd, an stressor, on renal cell ferroptosis. Transcriptomics analyses showed arachidonic acid (ARA) metabolic pathway was disrupted in Cd-exposed mouse kidneys. Targeted metabolomics oxidized ARA metabolites were increased mice. Renal 4-HNE, MDA, and ACSL4, upregulated Consistent with animal experiments, vitro experiments mitochondrial lipids elevated HK-2 cells. Ultrastructure membrane rupture Mitochondrial cristae accordingly reduced SIRT3, NAD