Lipid storage and lipophagy regulates ferroptosis

The synthesis, storage, and degradation of lipids are highly regulated processes. Impaired lipid metabolism is implicated in inflammation and cell death. Although ferroptosis is a recently described form of regulated cell death driven by lipid peroxidation, the impact of lipid droplets on ferroptosi...

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Published in	Biochemical and biophysical research communications Vol. 508; no. 4; pp. 997 - 1003
Main Authors	Bai, Yuansong, Meng, Lingjun, Han, Leng, Jia, Yuanyuan, Zhao, Yanan, Gao, Huan, Kang, Rui, Wang, Xiaofeng, Tang, Daolin, Dai, Enyong
Format	Journal Article
Language	English
Published	United States Elsevier Inc 22.01.2019
Subjects	antioxidants Autophagy cell death droplets Ferroptosis hepatocytes humans inflammation Lipid degradation Lipid droplets lipid metabolism lipid peroxidation Lipid storage lipids mice TPD52 NFE2L2/NRF2 GPX4 Lipid droplets ALOX15 NCOA4 STAT3 Lipid storage Ferroptosis ACSL4 MDA SLC7A11 Autophagy RCD TBA Lipid degradation 4-HNE ATG mHep LPCAT3 LD AMPK PLIN2
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Abstract	The synthesis, storage, and degradation of lipids are highly regulated processes. Impaired lipid metabolism is implicated in inflammation and cell death. Although ferroptosis is a recently described form of regulated cell death driven by lipid peroxidation, the impact of lipid droplets on ferroptosis remains unidentified. Here, we demonstrate that lipophagy, the autophagic degradation of intracellular lipid droplets, promotes RSL3-induced ferroptotic cell death in hepatocytes. Lipid droplet accumulation is increased at the early stage but decreased at the late stage of ferroptosis in mouse or human hepatocytes. Importantly, either genetically enhancing TPD52-dependent lipid storage or blocking ATG5-and RAB7A-dependent lipid degradation prevents RSL3-induced lipid peroxidation and subsequent ferroptosis in vitro and in vivo. These studies support an antioxidant role for lipid droplets in cell death and suggest novel strategies for the inhibition of ferroptosis by targeting the lipophagy pathway.
AbstractList	The synthesis, storage, and degradation of lipids are highly regulated processes. Impaired lipid metabolism is implicated in inflammation and cell death. Although ferroptosis is a recently described form of regulated cell death driven by lipid peroxidation, the impact of lipid droplets on ferroptosis remains unidentified. Here, we demonstrate that lipophagy, the autophagic degradation of intracellular lipid droplets, promotes RSL3-induced ferroptotic cell death in hepatocytes. Lipid droplet accumulation is increased at the early stage but decreased at the late stage of ferroptosis in mouse or human hepatocytes. Importantly, either genetically enhancing TPD52-dependent lipid storage or blocking ATG5-and RAB7A-dependent lipid degradation prevents RSL3-induced lipid peroxidation and subsequent ferroptosis in vitro and in vivo. These studies support an antioxidant role for lipid droplets in cell death and suggest novel strategies for the inhibition of ferroptosis by targeting the lipophagy pathway.The synthesis, storage, and degradation of lipids are highly regulated processes. Impaired lipid metabolism is implicated in inflammation and cell death. Although ferroptosis is a recently described form of regulated cell death driven by lipid peroxidation, the impact of lipid droplets on ferroptosis remains unidentified. Here, we demonstrate that lipophagy, the autophagic degradation of intracellular lipid droplets, promotes RSL3-induced ferroptotic cell death in hepatocytes. Lipid droplet accumulation is increased at the early stage but decreased at the late stage of ferroptosis in mouse or human hepatocytes. Importantly, either genetically enhancing TPD52-dependent lipid storage or blocking ATG5-and RAB7A-dependent lipid degradation prevents RSL3-induced lipid peroxidation and subsequent ferroptosis in vitro and in vivo. These studies support an antioxidant role for lipid droplets in cell death and suggest novel strategies for the inhibition of ferroptosis by targeting the lipophagy pathway. The synthesis, storage, and degradation of lipids are highly regulated processes. Impaired lipid metabolism is implicated in inflammation and cell death. Although ferroptosis is a recently described form of regulated cell death driven by lipid peroxidation, the impact of lipid droplets on ferroptosis remains unidentified. Here, we demonstrate that lipophagy, the autophagic degradation of intracellular lipid droplets, promotes RSL3-induced ferroptotic cell death in hepatocytes. Lipid droplet accumulation is increased at the early stage but decreased at the late stage of ferroptosis in mouse or human hepatocytes. Importantly, either genetically enhancing TPD52-dependent lipid storage or blocking ATG5-and RAB7A-dependent lipid degradation prevents RSL3-induced lipid peroxidation and subsequent ferroptosis in vitro and in vivo. These studies support an antioxidant role for lipid droplets in cell death and suggest novel strategies for the inhibition of ferroptosis by targeting the lipophagy pathway. The synthesis, storage, and degradation of lipids are highly regulated processes. Impaired lipid metabolism is implicated in inflammation and cell death. Although ferroptosis is a recently described form of regulated cell death driven by lipid peroxidation, the impact of lipid droplets on ferroptosis remains unidentified. Here, we demonstrate that lipophagy, the autophagic degradation of intracellular lipid droplets, promotes RSL3-induced ferroptotic cell death in hepatocytes. Lipid droplet accumulation is increased at the early stage but decreased at the late stage of ferroptosis in mouse or human hepatocytes. Importantly, either genetically enhancing TPD52-dependent lipid storage or blocking ATG5-and RAB7A-dependent lipid degradation prevents RSL3-induced lipid peroxidation and subsequent ferroptosis in vitro and in vivo. These studies support an antioxidant role for lipid droplets in cell death and suggest novel strategies for the inhibition of ferroptosis by targeting the lipophagy pathway.
Author	Bai, Yuansong Han, Leng Tang, Daolin Meng, Lingjun Jia, Yuanyuan Gao, Huan Kang, Rui Zhao, Yanan Wang, Xiaofeng Dai, Enyong
Author_xml	– sequence: 1 givenname: Yuansong surname: Bai fullname: Bai, Yuansong organization: Department of Oncology and Hematology, China-Japan Union Hospital of Jilin University, Changchun, Jilin, 130033, China – sequence: 2 givenname: Lingjun surname: Meng fullname: Meng, Lingjun organization: Department of Oncology and Hematology, China-Japan Union Hospital of Jilin University, Changchun, Jilin, 130033, China – sequence: 3 givenname: Leng surname: Han fullname: Han, Leng organization: Department of Oncology and Hematology, China-Japan Union Hospital of Jilin University, Changchun, Jilin, 130033, China – sequence: 4 givenname: Yuanyuan surname: Jia fullname: Jia, Yuanyuan organization: Department of Oncology and Hematology, China-Japan Union Hospital of Jilin University, Changchun, Jilin, 130033, China – sequence: 5 givenname: Yanan surname: Zhao fullname: Zhao, Yanan organization: Department of Oncology and Hematology, China-Japan Union Hospital of Jilin University, Changchun, Jilin, 130033, China – sequence: 6 givenname: Huan surname: Gao fullname: Gao, Huan organization: Department of Oncology and Hematology, China-Japan Union Hospital of Jilin University, Changchun, Jilin, 130033, China – sequence: 7 givenname: Rui surname: Kang fullname: Kang, Rui organization: Department of Surgery, UT Southwestern Medical Center, Dallas, TX, 75390, USA – sequence: 8 givenname: Xiaofeng surname: Wang fullname: Wang, Xiaofeng email: wangxiaofeng@jlu.edu.cn organization: Department of Stomatology, China-Japan Union Hospital of Jilin University, Changchun, Jilin, 130033, China – sequence: 9 givenname: Daolin orcidid: 0000-0002-1903-6180 surname: Tang fullname: Tang, Daolin email: daolin.tang@utsouthwestern.edu organization: Department of Surgery, UT Southwestern Medical Center, Dallas, TX, 75390, USA – sequence: 10 givenname: Enyong surname: Dai fullname: Dai, Enyong email: daienyong@yeah.net organization: Department of Oncology and Hematology, China-Japan Union Hospital of Jilin University, Changchun, Jilin, 130033, China
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/30545638$$D View this record in MEDLINE/PubMed
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Snippet	The synthesis, storage, and degradation of lipids are highly regulated processes. Impaired lipid metabolism is implicated in inflammation and cell death....
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SubjectTerms	antioxidants Autophagy cell death droplets Ferroptosis hepatocytes humans inflammation Lipid degradation Lipid droplets lipid metabolism lipid peroxidation Lipid storage lipids mice
Title	Lipid storage and lipophagy regulates ferroptosis
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