Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease

Publication date: 5 October 2017 Source:Cell, Volume 171, Issue 2 Author(s): Brent R. Stockwell, José Pedro Friedmann Angeli, Hülya Bayir, Ashley I. Bush, Marcus Conrad, Scott J. Dixon, Simone Fulda, Sergio Gascón, Stavroula K. Hatzios, Valerian E. Kagan, Kay Noel, Xuejun Jiang, Andreas Linkermann, Maureen E. Murphy, Michael Overholtzer, Atsushi Oyagi, Gabriela C. Pagnussat, Jason Park, Qitao Ran, Craig S. Rosenfeld, Konstantin Salnikow, Daolin Tang, Frank M. Torti, Suzy V. Torti, Shinya Toyokuni, K.A. Woerpel, Donna D. Zhang Ferroptosis is a form of regulated cell death characterized by the iron-dependent accumulation of lipid hydroperoxides to lethal levels. Emerging evidence suggests that ferroptosis represents an ancient vulnerability caused by the incorporation of polyunsaturated fatty acids into cellular membranes, and cells have developed complex systems that exploit and defend against this vulnerability in different contexts. The sensitivity to ferroptosis is tightly linked to numerous biological processes, including amino acid, iron, and polyunsaturated fatty acid metabolism, and the biosynthesis of glutathione, phospholipids, NADPH, and coenzyme Q10. Ferroptosis has been implicated in the pathological cell death associated with degenerative diseases (i.e., Alzheimer’s, Huntington’s, and Parkinson’s diseases), carcinogenesis, stroke, intracerebral hemorrhage, traumatic brain injury, ischemia-reperfusion injury, and kidney degener...
Source: Cell - Category: Cytology Source Type: research