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Title:
Ferroptosis: From regulation of lipid peroxidation to the treatment of diseases | Cell Biology and Toxicology
Description:
Ferroptosis is a regulated cell death mainly manifested by iron-dependent lipid peroxide accumulation. The leading cause of ferroptosis is the imbalance of intracellular oxidative systems (e.g., LOXs, POR, ROS) and antioxidant systems (e.g., GSH/GPx4, CoQ10/FSP1, BH4/GCH1), which is regulated by a complex network. In the past decade, this metabolic network has been continuously refined, and the links with various pathophysiological processes have been gradually established. Apoptosis has been regarded as the only form of regulated cell death for a long time, and the application of chemotherapeutic drugs to induce apoptosis of cancer cells is the mainstream method. However, studies have reported that cancer cells’ key features are resistance to apoptosis and chemotherapeutics. For high proliferation, cancer cells often have very active lipid metabolism and iron metabolism, which pave the way for ferroptosis. Interestingly, researchers found that drug-resistant or highly aggressive cancer cells are more prone to ferroptosis. Therefore, ferroptosis may be a potential strategy to eliminate cancer cells. In addition, links between ferroptosis and other diseases, such as neurological disorders and ischemia–reperfusion injury, have also been found. Understanding these diseases from the perspective of ferroptosis may provide new insights into clinical treatment. Herein, the metabolic processes in ferroptosis are reviewed, and the potential mechanisms and targets of ferroptosis in different diseases are summarized. Graphical Abstract
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Keywords {🔍}

pubmed, article, google, scholar, cas, ferroptosis, cell, cancer, central, death, wang, cells, iron, zhang, biol, role, res, chen, lipid, metabolism, injury, acid, mechanisms, disease, liu, glutathione, tang, ischemiareperfusion, med, mol, sci, sun, apoptosis, nature, biochem, yang, diseases, fatty, renal, kang, nat, zhao, treatment, oxidative, resistance, pharmacol, zhu, kroemer, chem, tumor,

Topics {✒️}

month download article/chapter escrt-iii-mediated membrane repair erastin/sorafenib induces cisplatin-resistant acyl-coa synthetase acsl4 myocardial ischemia-reperfusion injury myocardial ischemia/reperfusion injury renal ischemia/reperfusion injury st-elevation–myocardial infarction hepatic ischemia-reperfusion injury induced caspase-dependent apoptosis hmg-coa reductase inhibitors suppress erastin-induced ferroptosis acute renal failure genotype-selective antitumor agents cystine transporter slc7a11/xct autophagy-dependent cell death active lipid metabolism mitochondria-specific transgenic overexpression sun yat-sen university er stress-independent ferroptosis acs central sci ferroptosis-mediated tissue injury iron exporter ferroportin/slc40a1 ferroptosis-resistant cell state glutathione-independent ferroptosis suppressor full article pdf ischemia–reperfusion injury ischemia-reperfusion injury abnormal tumor metabolism article cell biology ferroptotic cell death acute kidney injury reactive oxygen species fatty acid metabolism glutathione redox system impaired lipid metabolism acetyl-coa carboxylase lpcat3 enriches arachidonate attenuates ischemia/reperfusion arachidonic acid metabolism friedmann angeli jp privacy choices/manage cookies sterol carrier protein-2 related subjects sulfasalazine-induced ferroptosis myocardial infarct size lipid peroxidase pathway intestinal ischemia/reperfusion bap1 tumor suppressor iron-dependent form

Questions {❓}

Emt and met in metastasis: where are the cancer stem cells?
Is membrane transport of FFA mediated by lipid, protein, or both?

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