Chen, Xin and Tsvetkov, Andrey S. and Shen, Han-Ming and Isidoro, Ciro and Ktistakis, Nicholas T. and Linkermann, Andreas and Koopman, Werner J. H. and Simon, Hans-Uwe and Galluzzi, Lorenzo and Luo, Shouqing and Xu, Daqian and Gu, Wei and Peulen, Olivier and Cai, Qian and Rubinsztein, David C. and Chi, Jen-Tsan and Zhang, Donna D. and Li, Changfeng and Toyokuni, Shinya and Liu, Jinbao and Roh, Jong-Lyel and Dai, Enyong and Juhász, Gábor and Liu, Wei and Zhang, Jianhua and Yang, Minghua and Liu, Jiao and Zhu, Ling-Qiang and Zou, Weiping and Piacentini, Mauro (2024) International consensus guidelines for the definition, detection, and interpretation of autophagy-dependent ferroptosis. AUTOPHAGY, 20 (6). pp. 1213-1246. ISSN 1554-8627
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Abstract
Macroautophagy/autophagy is a complex degradation process with a dual role in cell death that is influenced by the cell types that are involved and the stressors they are exposed to. Ferroptosis is an iron-dependent oxidative form of cell death characterized by unrestricted lipid peroxidation in the context of heterogeneous and plastic mechanisms. Recent studies have shed light on the involvement of specific types of autophagy (e.g. ferritinophagy, lipophagy, and clockophagy) in initiating or executing ferroptotic cell death through the selective degradation of anti-injury proteins or organelles. Conversely, other forms of selective autophagy (e.g. reticulophagy and lysophagy) enhance the cellular defense against ferroptotic damage. Dysregulated autophagy-dependent ferroptosis has implications for a diverse range of pathological conditions. This review aims to present an updated definition of autophagy-dependent ferroptosis, discuss influential substrates and receptors, outline experimental methods, and propose guidelines for interpreting the results.Abbreviation: 3-MA:3-methyladenine; 4HNE: 4-hydroxynonenal; ACD: accidentalcell death; ADF: autophagy-dependentferroptosis; ARE: antioxidant response element; BH2:dihydrobiopterin; BH4: tetrahydrobiopterin; BMDMs: bonemarrow-derived macrophages; CMA: chaperone-mediated autophagy; CQ:chloroquine; DAMPs: danger/damage-associated molecular patterns; EMT,epithelial-mesenchymal transition; EPR: electronparamagnetic resonance; ER, endoplasmic reticulum; FRET: Forsterresonance energy transfer; GFP: green fluorescent protein;GSH: glutathione;IF: immunofluorescence; IHC: immunohistochemistry; IOP, intraocularpressure; IRI: ischemia-reperfusion injury; LAA: linoleamide alkyne;MDA: malondialdehyde; PGSK: Phen Green (TM) SK;RCD: regulatedcell death; PUFAs: polyunsaturated fatty acids; RFP: red fluorescentprotein;ROS: reactive oxygen species; TBA: thiobarbituricacid; TBARS: thiobarbituric acid reactive substances; TEM:transmission electron microscopy.
| Item Type: | Article |
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| Additional Information: | Funding Agency and Grant Number: National Natural Science Foundation of China [82272660]; Plan on Enhancing Scientific Research in GMU [02-410-2302289XM]; National Institutes of Health [NIH] of USA [R01CA160417, R01CA229275, R01CA211070]; NIH [GM131919]; Ligue contre le Cancer [equipe labellisee]; Agence National de la Recherche [ANR]; AMMICa US23/CNRS [UMS3655]; Association pour la recherche sur le cancer [ARC]; Canceropple Ile-de-France; Fondation pour la Recherche Medicale [FRM]; European Joint Programme on Rare Diseases (EJPRD); European Research Council Advanced Investigator Award [101052444]; European Union Horizon 2020 Projects Oncobiome, Prevalung [101095604]; Crimson; Fondation Carrefour; Institut National du Cancer [INCa]; Institut Universitaire de France; LabEx Immuno-Oncology [ANR-18- IDEX-0001]; Mark Foundation; RHU Immunolife; Seerave Foundation; SIRIC Stratified Oncology Cell DNA Repair and Tumor Immune Elimination [SOCRATE]; SIRIC Cancer Research and Personalized Medicine [CARPEM]; IdEx Universite de Paris [ANR-18-IDEX-0001] Funding text: The work was supported by the National Natural Science Foundation of China [82272660]. X.C. was supported by the Plan on Enhancing Scientific Research in GMU [02-410-2302289XM] and the National Natural Science Foundation of China [82272660]. D.T. was supported by grants from the National Institutes of Health [NIH] of USA [R01CA160417, R01CA229275, and R01CA211070]. D.J.K. was supported by NIH grant GM131919. G.K. is supported by the Ligue contre le Cancer [equipe labellisee]; Agence National de la Recherche [ANR] - Projets blancs; AMMICa US23/CNRS UMS3655; Association pour la recherche sur le cancer [ARC]; Canceropple Ile-de-France; Fondation pour la Recherche Medicale [FRM]; a donation by Elior; Equipex Onco- Pheno-Screen; European Joint Programme on Rare Diseases (EJPRD); European Research Council Advanced Investigator Award [ERC-2021- ADG, ICD-Cancer, Grant No. 101052444], European Union Horizon 2020 Projects Oncobiome, Prevalung [grant No. 101095604] and Crimson; Fondation Carrefour; Institut National du Cancer [INCa]; Institut Universitaire de France; LabEx Immuno-Oncology [ANR-18- IDEX-0001]; a Cancer Research ASPIRE Award from the Mark Foundation; the RHU Immunolife; Seerave Foundation; SIRIC Stratified Oncology Cell DNA Repair and Tumor Immune Elimination [SOCRATE]; and SIRIC Cancer Research and Personalized Medicine [CARPEM]. This study contributes to the IdEx Universite de Paris ANR-18-IDEX-0001. |
| Uncontrolled Keywords: | LIPID-PEROXIDATION; MASS-SPECTROMETRY; PROTEIN; CANCER-CELLS; Lipid Peroxidation; IRON; Cell Death; acute kidney injury; transcription factor Nrf2; Lipophagy; ferritinophagy; ferritinophagy; ERASTIN-INDUCED FERROPTOSIS; NONAPOPTOTIC CELL-DEATH; |
| Subjects: | Q Science / természettudomány > QH Natural history / természetrajz > QH301 Biology / biológia |
| SWORD Depositor: | MTMT SWORD |
| Depositing User: | MTMT SWORD |
| Date Deposited: | 24 Jan 2025 10:45 |
| Last Modified: | 24 Jan 2025 10:45 |
| URI: | https://real.mtak.hu/id/eprint/214314 |
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