{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Mann J"],"funding":["NCI NIH HHS","NIH HHS"],"pagination":["249-264.e7"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10922137"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["31(2)"],"pubmed_abstract":["Iron overload, characterized by accumulation of iron in tissues, induces a multiorgan toxicity whose mechanisms are not fully understood. Using cultured cell lines, Caenorhabditis elegans, and mice, we found that ferroptosis occurs in the context of iron-overload-mediated damage. Exogenous oleic acid protected against iron-overload-toxicity in cell culture and Caenorhabditis elegans by suppressing ferroptosis. In mice, oleic acid protected against FAC-induced liver lipid peroxidation and damage. Oleic acid changed the cellular lipid composition, characterized by decreased levels of polyunsaturated fatty acyl phospholipids and decreased levels of ether-linked phospholipids. The protective effect of oleic acid in cells was attenuated by GW6471 (PPAR-α antagonist), as well as in Caenorhabditis elegans lacking the nuclear hormone receptor NHR-49 (a PPAR-α functional homologue). These results highlight ferroptosis as a driver of iron-overload-mediated damage, which is inhibited by oleic acid. This monounsaturated fatty acid represents a potential therapeutic approach to mitigating organ damage in iron overload individuals."],"journal":["Cell chemical biology"],"pubmed_title":["Ferroptosis inhibition by oleic acid mitigates iron-overload-induced injury."],"pmcid":["PMC10922137"],"funding_grant_id":["R35 CA209896","P40 OD010440","P30 CA013696"],"pubmed_authors":["Fongheiser MA","Dafre AL","Farina M","Mann J","Smith N","Hirschhorn T","Stockwell BR","Miranda-Vizuete A","Reznik E","Santer M","Zandkarimi F","Soni RK"],"additional_accession":[]},"is_claimable":false,"name":"Ferroptosis inhibition by oleic acid mitigates iron-overload-induced injury.","description":"Iron overload, characterized by accumulation of iron in tissues, induces a multiorgan toxicity whose mechanisms are not fully understood. Using cultured cell lines, Caenorhabditis elegans, and mice, we found that ferroptosis occurs in the context of iron-overload-mediated damage. Exogenous oleic acid protected against iron-overload-toxicity in cell culture and Caenorhabditis elegans by suppressing ferroptosis. In mice, oleic acid protected against FAC-induced liver lipid peroxidation and damage. Oleic acid changed the cellular lipid composition, characterized by decreased levels of polyunsaturated fatty acyl phospholipids and decreased levels of ether-linked phospholipids. The protective effect of oleic acid in cells was attenuated by GW6471 (PPAR-α antagonist), as well as in Caenorhabditis elegans lacking the nuclear hormone receptor NHR-49 (a PPAR-α functional homologue). These results highlight ferroptosis as a driver of iron-overload-mediated damage, which is inhibited by oleic acid. This monounsaturated fatty acid represents a potential therapeutic approach to mitigating organ damage in iron overload individuals.","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Feb","modification":"2026-06-01T21:06:07.249Z","creation":"2025-04-20T01:50:19.276Z"},"accession":"S-EPMC10922137","cross_references":{"pubmed":["37944523"],"doi":["10.1016/j.chembiol.2023.10.012"]}}