Tau-mediated iron export prevents ferroptotic damage after ischemic stroke
By Qing-zhang Tuo, Peng Lei, Katherine A. Jackman, Li Xl, H. Xiong, Zhen-yu Liuyang, Laila C. Roisman, Z. St, Scott Ayton, Qiang Wang and 10 more. Molecular Psychiatry, 2017
614 citations recorded by the source corpus.
Subfields: Molecular Biology, Physiology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/57d4a86ddb608c0facf4d9f2e815ab54378739c6
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In Pulmonary and Respiratory Medicine
Citations in the corpus
- Ferroptosis: mechanisms and links with diseases (2021, background): “I/R in the brain can acutely suppress tau expression, an Alzheimer’s disease protein that can facilitate iron export,(278,279) causing iron accumulation accompanied by ferroptosis in the infarct zone, which aggravated neuronal damage.(262) Iron chelation and ferrostatin-1 have similar protective eff”
- Mechanisms of neuronal cell death in ischemic stroke and their therapeutic implications (2021, background): “The process also causes intracellular accumulation of redox‐active iron.(184) Ultimately, all of these may collectively”
- Ferroptosis as a target for protection against cardiomyopathy (2019, background): “Ferroptosis has been implicated in the pathological process associated with carcinogenesis, degenerative diseases, stroke, and kidney ischemia/reperfusion (I/R) injury (5, 6).”
- Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease. (2017, neutral): “Inhibitors of ferroptosis, such as ferrostatins and liproxstatins, protect from ischemic injury in mouse models in the liver, kidney, brain, and heart (Friedmann Angeli et al., 2014; Gao et al., 2015; Linkermann et al., 2014; Skouta et al., 2014; Tuo et al., 2017).”