{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Liu Z"],"funding":["Biotechnology and Biological Sciences Research Council"],"pagination":["1106693"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10294229"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14"],"pubmed_abstract":["Patients with occupational medicamentose-like dermatitis due to trichloroethylene often suffer from immune kidney injury. Our previous study reveals that C5b-9-dependent cytosolic Ca<sup>2+</sup> overload-induced ferroptosis is involved in trichloroethylene sensitized kidney injury. However, how C5b-9 causes cytosolic Ca<sup>2+</sup> rise and the specific mechanism whereby overloaded Ca<sup>2+</sup> induces ferroptosis remain unknown. The purpose of our study was to explore the role of IP3R-dependent mitochondrial dysfunction in C5b-9 mediated ferroptosis in trichloroethylene sensitized kidney. Our results showed that IP3R was activated, and mitochondrial membrane potential was decreased in the renal epithelial cells of trichloroethylene-sensitized mice, and these changes were antagonized "],"journal":["Frontiers in immunology"],"pubmed_title":["IP3R-dependent mitochondrial dysfunction mediates C5b-9-induced ferroptosis in trichloroethylene-caused immune kidney injury."],"pmcid":["PMC10294229"],"funding_grant_id":["BB/P004695/1"],"pubmed_authors":["Liu Z","Xie H","Zhang J","Zuo X","Zhang X","Wu C","Wang F","Ma J","Zhu Q"],"additional_accession":[]},"is_claimable":false,"name":"IP3R-dependent mitochondrial dysfunction mediates C5b-9-induced ferroptosis in trichloroethylene-caused immune kidney injury.","description":"Patients with occupational medicamentose-like dermatitis due to trichloroethylene often suffer from immune kidney injury. Our previous study reveals that C5b-9-dependent cytosolic Ca<sup>2+</sup> overload-induced ferroptosis is involved in trichloroethylene sensitized kidney injury. However, how C5b-9 causes cytosolic Ca<sup>2+</sup> rise and the specific mechanism whereby overloaded Ca<sup>2+</sup> induces ferroptosis remain unknown. The purpose of our study was to explore the role of IP3R-dependent mitochondrial dysfunction in C5b-9 mediated ferroptosis in trichloroethylene sensitized kidney. Our results showed that IP3R was activated, and mitochondrial membrane potential was decreased in the renal epithelial cells of trichloroethylene-sensitized mice, and these changes were antagonized ","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023","modification":"2025-04-04T12:11:31.034Z","creation":"2025-04-04T12:11:31.034Z"},"accession":"S-EPMC10294229","cross_references":{"pubmed":["37383224"],"doi":["10.3389/fimmu.2023.1106693"]}}