<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Liu Z</submitter><funding>Biotechnology and Biological Sciences Research Council</funding><pagination>1106693</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10294229</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14</volume><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&lt;sup>2+&lt;/sup> overload-induced ferroptosis is involved in trichloroethylene sensitized kidney injury. However, how C5b-9 causes cytosolic Ca&lt;sup>2+&lt;/sup> rise and the specific mechanism whereby overloaded Ca&lt;sup>2+&lt;/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 </pubmed_abstract><journal>Frontiers in immunology</journal><pubmed_title>IP3R-dependent mitochondrial dysfunction mediates C5b-9-induced ferroptosis in trichloroethylene-caused immune kidney injury.</pubmed_title><pmcid>PMC10294229</pmcid><funding_grant_id>BB/P004695/1</funding_grant_id><pubmed_authors>Liu Z</pubmed_authors><pubmed_authors>Xie H</pubmed_authors><pubmed_authors>Zhang J</pubmed_authors><pubmed_authors>Zuo X</pubmed_authors><pubmed_authors>Zhang X</pubmed_authors><pubmed_authors>Wu C</pubmed_authors><pubmed_authors>Wang F</pubmed_authors><pubmed_authors>Ma J</pubmed_authors><pubmed_authors>Zhu Q</pubmed_authors></additional><is_claimable>false</is_claimable><name>IP3R-dependent mitochondrial dysfunction mediates C5b-9-induced ferroptosis in trichloroethylene-caused immune kidney injury.</name><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&lt;sup>2+&lt;/sup> overload-induced ferroptosis is involved in trichloroethylene sensitized kidney injury. However, how C5b-9 causes cytosolic Ca&lt;sup>2+&lt;/sup> rise and the specific mechanism whereby overloaded Ca&lt;sup>2+&lt;/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 </description><dates><release>2023-01-01T00:00:00Z</release><publication>2023</publication><modification>2025-04-04T12:11:31.034Z</modification><creation>2025-04-04T12:11:31.034Z</creation></dates><accession>S-EPMC10294229</accession><cross_references><pubmed>37383224</pubmed><doi>10.3389/fimmu.2023.1106693</doi></cross_references></HashMap>