TY - JOUR
T1 - Autophagy-Dependent Ferroptosis
T2 - Machinery and Regulation
AU - Liu, Jiao
AU - Kuang, Feimei
AU - Kroemer, Guido
AU - Klionsky, Daniel J.
AU - Kang, Rui
AU - Tang, Daolin
N1 - Funding Information:
We apologize to the researchers who were not referenced due to space limitations. We thank Dave Primm (Department of Surgery, University of Texas Southwestern Medical Center) for his critical reading of the manuscript. This work was supported by grants from the US NIH ( GM131919 to D.J.K.) and the American Cancer Society (Research Scholar Grant RSG-16-014-01-CDD to D.T.). G.K. is supported by the Ligue Contre le Cancer (équipe labellisée); Agence National de la Recherche (ANR)––Projets blancs; ANR under the frame of E-Rare-2, the ERA-Net for Research on Rare Diseases ; Association pour la Recherche sur le Cancer (ARC); Cancéropôle Île-de-France ; Chancelerie des universités de Paris (Legs Poix), Fondation pour la Recherche Médicale (FRM); a donation by Elior ; European Research Area Network on Cardiovascular Diseases (ERA-CVD, MINOTAUR); the European Union Horizon 2020 Project Oncobiome; Fondation Carrefour ; Institut National Du Cancer (INCa); Inserm (HTE); Institut Universitaire de France ; Leducq Foundation ; the LabEx Immuno-Oncology ; the RHU Torino Lumière ; the Seattle Foundation ; the SIRIC Stratified Oncology Cell DNA Repair and Tumor Immune Elimination ( SOCRATE ); and the SIRIC Cancer Research and Personalized Medicine ( CARPEM ). J.L. is supported by grants from the National Natural Science Foundation of China ( 31671435 , 81400132 , and 81772508 ).
Publisher Copyright:
© 2020 Elsevier Ltd
PY - 2020/4/16
Y1 - 2020/4/16
N2 - Macroautophagy (hereafter referred to as autophagy) is an evolutionarily conserved cellular process capable of degrading various biological molecules (e.g., protein, glycogen, lipids, DNA, and RNA) and organelles (e.g., mitochondria, endoplasmic reticulum [ER] ribosomes, lysosomes, and micronuclei) via the lysosomal pathway. Ferroptosis is a type of oxidative stress-dependent regulated cell death associated with iron accumulation and lipid peroxidation. The recently discovered role of autophagy, especially selective types of autophagy (e.g., ferritinophagy, lipophagy, clockophagy, and chaperone-mediated autophagy), in driving cells toward ferroptotic death motivated us to explore the functional interactions between metabolism, immunity, and cell death. Here, we describe types of selective autophagy and discuss the regulatory mechanisms and signaling pathways of autophagy-dependent ferroptosis. We also summarize chemical modulators that are currently available for triggering or blocking autophagy-dependent ferroptosis and that may be developed for therapeutic interventions in human diseases.
AB - Macroautophagy (hereafter referred to as autophagy) is an evolutionarily conserved cellular process capable of degrading various biological molecules (e.g., protein, glycogen, lipids, DNA, and RNA) and organelles (e.g., mitochondria, endoplasmic reticulum [ER] ribosomes, lysosomes, and micronuclei) via the lysosomal pathway. Ferroptosis is a type of oxidative stress-dependent regulated cell death associated with iron accumulation and lipid peroxidation. The recently discovered role of autophagy, especially selective types of autophagy (e.g., ferritinophagy, lipophagy, clockophagy, and chaperone-mediated autophagy), in driving cells toward ferroptotic death motivated us to explore the functional interactions between metabolism, immunity, and cell death. Here, we describe types of selective autophagy and discuss the regulatory mechanisms and signaling pathways of autophagy-dependent ferroptosis. We also summarize chemical modulators that are currently available for triggering or blocking autophagy-dependent ferroptosis and that may be developed for therapeutic interventions in human diseases.
KW - autophagy
KW - ferroptosis
KW - network
KW - regulated cell death
KW - selective autophagy
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U2 - 10.1016/j.chembiol.2020.02.005
DO - 10.1016/j.chembiol.2020.02.005
M3 - Review article
C2 - 32160513
AN - SCOPUS:85082976935
SN - 2451-9456
VL - 27
SP - 420
EP - 435
JO - Cell Chemical Biology
JF - Cell Chemical Biology
IS - 4
ER -