Nature, Journal Year: 2020, Volume and Issue: 585(7826), P. 603 - 608
Published: Sept. 16, 2020
Language: Английский
Nature Reviews Molecular Cell Biology, Journal Year: 2021, Volume and Issue: 22(4), P. 266 - 282
Published: Jan. 25, 2021
Language: Английский
Citations
4434
Cell Death and Disease, Journal Year: 2020, Volume and Issue: 11(2)
Published: Feb. 3, 2020
Abstract Ferroptosis is a new type of cell death that was discovered in recent years and usually accompanied by large amount iron accumulation lipid peroxidation during the process; occurrence ferroptosis iron-dependent. Ferroptosis-inducing factors can directly or indirectly affect glutathione peroxidase through different pathways, resulting decrease antioxidant capacity reactive oxygen species (ROS) cells, ultimately leading to oxidative death. Recent studies have shown closely related pathophysiological processes many diseases, such as tumors, nervous system ischemia-reperfusion injury, kidney blood diseases. How intervene development diseases regulating has become hotspot focus etiological research treatment, but functional changes specific molecular mechanisms still need be further explored. This paper systematically summarizes latest progress research, with on providing references for understanding its pathogenesis proposing targets treatment
Language: Английский
Citations
2944
Nature, Journal Year: 2019, Volume and Issue: 575(7784), P. 688 - 692
Published: Oct. 21, 2019
Language: Английский
Citations
2634
Cell Research, Journal Year: 2020, Volume and Issue: 31(2), P. 107 - 125
Published: Dec. 2, 2020
Abstract Cell death can be executed through different subroutines. Since the description of ferroptosis as an iron-dependent form non-apoptotic cell in 2012, there has been mounting interest process and function ferroptosis. Ferroptosis occur two major pathways, extrinsic or transporter-dependent pathway intrinsic enzyme-regulated pathway. is caused by a redox imbalance between production oxidants antioxidants, which driven abnormal expression activity multiple redox-active enzymes that produce detoxify free radicals lipid oxidation products. Accordingly, precisely regulated at levels, including epigenetic, transcriptional, posttranscriptional posttranslational layers. The transcription factor NFE2L2 plays central role upregulating anti-ferroptotic defense, whereas selective autophagy may promote ferroptotic death. Here, we review current knowledge on integrated molecular machinery describe how dysregulated involved cancer, neurodegeneration, tissue injury, inflammation, infection.
Language: Английский
Citations
2580
Nature Reviews Clinical Oncology, Journal Year: 2021, Volume and Issue: 18(5), P. 280 - 296
Published: Jan. 29, 2021
Language: Английский
Citations
2034
Cell, Journal Year: 2022, Volume and Issue: 185(14), P. 2401 - 2421
Published: July 1, 2022
Ferroptosis, a form of cell death driven by iron-dependent lipid peroxidation, was identified as distinct phenomenon and named decade ago. Ferroptosis has been implicated in broad set biological contexts, from development to aging, immunity, cancer. This review describes key regulators this within framework metabolism, ROS biology, iron biology. Key concepts major unanswered questions the ferroptosis field are highlighted. The next promises yield further breakthroughs mechanisms governing additional ways harnessing for therapeutic benefit.
Language: Английский
Citations
1726
Nature reviews. Cancer, Journal Year: 2022, Volume and Issue: 22(7), P. 381 - 396
Published: March 25, 2022
Language: Английский
Citations
1446
Autophagy, Journal Year: 2020, Volume and Issue: 17(9), P. 2054 - 2081
Published: Aug. 19, 2020
Ferroptosis is an iron-dependent, non-apoptotic form of regulated cell death caused by lipid peroxidation, which controlled integrated oxidation and antioxidant systems. The iron-containing enzyme lipoxygenase the main promoter ferroptosis producing hydroperoxides, its function relies on activation ACSL4-dependent biosynthesis. In contrast, selenium-containing GPX4 currently recognized as a central repressor ferroptosis, activity depends glutathione produced from cystine-glutamate antiporter SLC7A11. Many metabolic (especially involving iron, lipids, amino acids) degradation pathways (macroautophagy/autophagy ubiquitin-proteasome system) orchestrate complex ferroptotic response through direct or indirect regulation iron accumulation peroxidation. Although detailed mechanism membrane injury during remains mystery, ESCRT III-mediated plasma repair can make cells resistant to ferroptosis. Here, we review recent rapid progress in understanding molecular mechanisms focus epigenetic, transcriptional, posttranslational this process.Abbreviations: 2ME: beta-mercaptoethanol; α-KG: α-ketoglutarate; ccRCC: clear renal carcinoma; EMT: epithelial-mesenchymal transition; FAO: fatty acid beta-oxidation; GSH: glutathione; MEFs: mouse embryonic fibroblasts; MUFAs: monounsaturated acids; NO: nitric oxide; NOX: NADPH oxidase; PPP: pentose phosphate pathway; PUFA: polyunsaturated acid; RCD: death; RNS: reactive nitrogen species; ROS: oxygen RTAs: radical-trapping antioxidants; UPS: system; UTR: untranslated region.
Language: Английский
Citations
1349
Free Radical Biology and Medicine, Journal Year: 2020, Volume and Issue: 152, P. 175 - 185
Published: March 9, 2020
Language: Английский
Citations
1283
Nature, Journal Year: 2021, Volume and Issue: 593(7860), P. 586 - 590
Published: May 12, 2021
Language: Английский
Citations
1257