<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Skouta R</submitter><funding>NICHD NIH HHS</funding><funding>NIDDK NIH HHS</funding><funding>NCRR NIH HHS</funding><funding>NCI NIH HHS</funding><funding>NINDS NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>4551-6</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3985476</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>136(12)</volume><pubmed_abstract>Ferrostatin-1 (Fer-1) inhibits ferroptosis, a form of regulated, oxidative, nonapoptotic cell death. We found that Fer-1 inhibited cell death in cellular models of Huntington's disease (HD), periventricular leukomalacia (PVL), and kidney dysfunction; Fer-1 inhibited lipid peroxidation, but not mitochondrial reactive oxygen species formation or lysosomal membrane permeability. We developed a mechanistic model to explain the activity of Fer-1, which guided the development of ferrostatins with improved properties. These studies suggest numerous therapeutic uses for ferrostatins, and that lipid peroxidation mediates diverse disease phenotypes.</pubmed_abstract><journal>Journal of the American Chemical Society</journal><pubmed_title>Ferrostatins inhibit oxidative lipid damage and cell death in diverse disease models.</pubmed_title><pmcid>PMC3985476</pmcid><funding_grant_id>R01 GM085081</funding_grant_id><funding_grant_id>DK34275</funding_grant_id><funding_grant_id>R01 DK034275</funding_grant_id><funding_grant_id>HD18655</funding_grant_id><funding_grant_id>R01 CA097061</funding_grant_id><funding_grant_id>R01CA097061</funding_grant_id><funding_grant_id>R56 DK034275</funding_grant_id><funding_grant_id>1S10RR025431-01A1</funding_grant_id><funding_grant_id>K99 CA166517</funding_grant_id><funding_grant_id>1K99CA166517-01</funding_grant_id><funding_grant_id>P30 HD018655</funding_grant_id><funding_grant_id>NS066019</funding_grant_id><funding_grant_id>R00 CA166517</funding_grant_id><funding_grant_id>R01 NS066019</funding_grant_id><funding_grant_id>R01 CA161061</funding_grant_id><funding_grant_id>R01GM085081</funding_grant_id><pubmed_authors>Skouta R</pubmed_authors><pubmed_authors>Stockwell BR</pubmed_authors><pubmed_authors>Orman M</pubmed_authors><pubmed_authors>Dixon SJ</pubmed_authors><pubmed_authors>Linkermann A</pubmed_authors><pubmed_authors>Rosenberg PA</pubmed_authors><pubmed_authors>Wang J</pubmed_authors><pubmed_authors>Lo DC</pubmed_authors><pubmed_authors>Shimada K</pubmed_authors><pubmed_authors>Dunn DE</pubmed_authors><pubmed_authors>Weinberg JM</pubmed_authors></additional><is_claimable>false</is_claimable><name>Ferrostatins inhibit oxidative lipid damage and cell death in diverse disease models.</name><description>Ferrostatin-1 (Fer-1) inhibits ferroptosis, a form of regulated, oxidative, nonapoptotic cell death. We found that Fer-1 inhibited cell death in cellular models of Huntington's disease (HD), periventricular leukomalacia (PVL), and kidney dysfunction; Fer-1 inhibited lipid peroxidation, but not mitochondrial reactive oxygen species formation or lysosomal membrane permeability. We developed a mechanistic model to explain the activity of Fer-1, which guided the development of ferrostatins with improved properties. These studies suggest numerous therapeutic uses for ferrostatins, and that lipid peroxidation mediates diverse disease phenotypes.</description><dates><release>2014-01-01T00:00:00Z</release><publication>2014 Mar</publication><modification>2021-02-21T08:20:24Z</modification><creation>2019-03-27T01:24:53Z</creation></dates><accession>S-EPMC3985476</accession><cross_references><pubmed>24592866</pubmed><doi>10.1021/ja411006a</doi></cross_references></HashMap>