Ferrostatins Inhibit Oxidative Lipid Damage and Cell Death in Diverse Disease Models

[Image: see text] 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 peroxidat...

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Autores principales: Skouta, Rachid, Dixon, Scott J., Wang, Jianlin, Dunn, Denise E., Orman, Marina, Shimada, Kenichi, Rosenberg, Paul A., Lo, Donald C., Weinberg, Joel M., Linkermann, Andreas, Stockwell, Brent R.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Chemical Society 2014
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3985476/
https://www.ncbi.nlm.nih.gov/pubmed/24592866
http://dx.doi.org/10.1021/ja411006a
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author Skouta, Rachid
Dixon, Scott J.
Wang, Jianlin
Dunn, Denise E.
Orman, Marina
Shimada, Kenichi
Rosenberg, Paul A.
Lo, Donald C.
Weinberg, Joel M.
Linkermann, Andreas
Stockwell, Brent R.
author_facet Skouta, Rachid
Dixon, Scott J.
Wang, Jianlin
Dunn, Denise E.
Orman, Marina
Shimada, Kenichi
Rosenberg, Paul A.
Lo, Donald C.
Weinberg, Joel M.
Linkermann, Andreas
Stockwell, Brent R.
author_sort Skouta, Rachid
collection PubMed
description [Image: see text] 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.
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spelling pubmed-39854762015-03-04 Ferrostatins Inhibit Oxidative Lipid Damage and Cell Death in Diverse Disease Models Skouta, Rachid Dixon, Scott J. Wang, Jianlin Dunn, Denise E. Orman, Marina Shimada, Kenichi Rosenberg, Paul A. Lo, Donald C. Weinberg, Joel M. Linkermann, Andreas Stockwell, Brent R. J Am Chem Soc [Image: see text] 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. American Chemical Society 2014-03-04 2014-03-26 /pmc/articles/PMC3985476/ /pubmed/24592866 http://dx.doi.org/10.1021/ja411006a Text en Copyright © 2014 American Chemical Society
spellingShingle Skouta, Rachid
Dixon, Scott J.
Wang, Jianlin
Dunn, Denise E.
Orman, Marina
Shimada, Kenichi
Rosenberg, Paul A.
Lo, Donald C.
Weinberg, Joel M.
Linkermann, Andreas
Stockwell, Brent R.
Ferrostatins Inhibit Oxidative Lipid Damage and Cell Death in Diverse Disease Models
title Ferrostatins Inhibit Oxidative Lipid Damage and Cell Death in Diverse Disease Models
title_full Ferrostatins Inhibit Oxidative Lipid Damage and Cell Death in Diverse Disease Models
title_fullStr Ferrostatins Inhibit Oxidative Lipid Damage and Cell Death in Diverse Disease Models
title_full_unstemmed Ferrostatins Inhibit Oxidative Lipid Damage and Cell Death in Diverse Disease Models
title_short Ferrostatins Inhibit Oxidative Lipid Damage and Cell Death in Diverse Disease Models
title_sort ferrostatins inhibit oxidative lipid damage and cell death in diverse disease models
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3985476/
https://www.ncbi.nlm.nih.gov/pubmed/24592866
http://dx.doi.org/10.1021/ja411006a
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