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Multiple functions of MLKL in liver fibrosis, from necroptosis to hepatic stellate cell activation.

作者信息

Pistorio Valeria, Housset Chantal, Gautheron Jérémie

机构信息

Department of Chemical Sciences, University of Naples Federico II, Naples, Italy.

Sorbonne Université, Inserm, Centre de Recherche Saint-Antoine (CRSA), Paris, France.

出版信息

Theranostics. 2022 Jul 25;12(13):5820-5823. doi: 10.7150/thno.76902. eCollection 2022.

DOI:10.7150/thno.76902
PMID:35966599
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9373804/
Abstract
摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9be/9373804/33c24e4529d3/thnov12p5820g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9be/9373804/33c24e4529d3/thnov12p5820g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9be/9373804/33c24e4529d3/thnov12p5820g001.jpg

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Multiple functions of MLKL in liver fibrosis, from necroptosis to hepatic stellate cell activation.混合谱系激酶结构域样蛋白（MLKL）在肝纤维化中的多种功能，从坏死性凋亡到肝星状细胞激活。
Theranostics. 2022 Jul 25;12(13):5820-5823. doi: 10.7150/thno.76902. eCollection 2022.
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Loss of MLKL ameliorates liver fibrosis by inhibiting hepatocyte necroptosis and hepatic stellate cell activation.MLKL 的缺失通过抑制肝细胞坏死性凋亡和肝星状细胞激活来改善肝纤维化。
Theranostics. 2022 Jul 4;12(11):5220-5236. doi: 10.7150/thno.71400. eCollection 2022.
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Curcumol induces RIPK1/RIPK3 complex-dependent necroptosis via JNK1/2-ROS signaling in hepatic stellate cells.姜黄素通过 JNK1/2-ROS 信号通路诱导肝星状细胞中 RIPK1/RIPK3 复合物依赖的坏死性凋亡。
Redox Biol. 2018 Oct;19:375-387. doi: 10.1016/j.redox.2018.09.007. Epub 2018 Sep 7.
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Receptor-Interacting Serine/Threonine-Protein Kinase 3 (RIPK3)-Mixed Lineage Kinase Domain-Like Protein (MLKL)-Mediated Necroptosis Contributes to Ischemia-Reperfusion Injury of Steatotic Livers.受体相互作用丝氨酸/苏氨酸蛋白激酶 3（RIPK3）-混合谱系激酶结构域样蛋白（MLKL）介导线粒体凋亡程序性坏死导致肝脂肪变性再灌注损伤。
Am J Pathol. 2019 Jul;189(7):1363-1374. doi: 10.1016/j.ajpath.2019.03.010. Epub 2019 Apr 23.
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RIP1, RIP3, and MLKL Contribute to Cell Death Caused by Clostridium perfringens Enterotoxin.RIP1、RIP3 和 MLKL 导致产气荚膜梭菌肠毒素引起的细胞死亡。
mBio. 2019 Dec 17;10(6):e02985-19. doi: 10.1128/mBio.02985-19.
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A cytosolic heat shock protein 90 and co-chaperone p23 complex activates RIPK3/MLKL during necroptosis of endothelial cells in acute respiratory distress syndrome.胞质热休克蛋白 90 和共伴侣 p23 复合物在急性呼吸窘迫综合征内皮细胞坏死性凋亡过程中激活 RIPK3/MLKL。
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The NS1 Protein of Influenza A Virus Participates in Necroptosis by Interacting with MLKL and Increasing Its Oligomerization and Membrane Translocation.甲型流感病毒 NS1 蛋白通过与 MLKL 相互作用并增加其寡聚化和膜转位来参与坏死性凋亡。
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MLKL trafficking and accumulation at the plasma membrane control the kinetics and threshold for necroptosis.MLKL 在质膜上的转运和聚集控制着细胞发生坏死性凋亡的动力学和阈值。
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Necroptosis: a crucial pathogenic mediator of human disease.细胞程序性坏死：人类疾病的关键致病介质。
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本文引用的文献

1
Loss of MLKL ameliorates liver fibrosis by inhibiting hepatocyte necroptosis and hepatic stellate cell activation.MLKL 的缺失通过抑制肝细胞坏死性凋亡和肝星状细胞激活来改善肝纤维化。
Theranostics. 2022 Jul 4;12(11):5220-5236. doi: 10.7150/thno.71400. eCollection 2022.
2
MLKL: Functions beyond serving as the Executioner of Necroptosis.MLKL：除了作为细胞坏死性凋亡的执行者之外的功能。
Theranostics. 2021 Mar 4;11(10):4759-4769. doi: 10.7150/thno.54072. eCollection 2021.
3
RIPK3 acts as a lipid metabolism regulator contributing to inflammation and carcinogenesis in non-alcoholic fatty liver disease.
Mediators of necroptosis: from cell death to metabolic regulation.
坏死性凋亡的介体：从细胞死亡到代谢调节。
EMBO Mol Med. 2024 Feb;16(2):219-237. doi: 10.1038/s44321-023-00011-z. Epub 2024 Jan 9.
4
Novel Inhibitor of Mixed-Lineage Kinase Domain-Like Protein: The Antifibrotic Effects of a Necroptosis Antagonist.混合谱系激酶结构域样蛋白的新型抑制剂：坏死性凋亡拮抗剂的抗纤维化作用
ACS Pharmacol Transl Sci. 2023 Sep 11;6(10):1471-1479. doi: 10.1021/acsptsci.3c00131. eCollection 2023 Oct 13.
5
Targeting Endothelial Necroptosis Disrupts Profibrotic Endothelial-Hepatic Stellate Cells Crosstalk to Alleviate Liver Fibrosis in Nonalcoholic Steatohepatitis.靶向内皮细胞坏死性凋亡可破坏非酒精性脂肪性肝炎中促纤维化内皮细胞-肝星状细胞的串扰，从而减轻肝纤维化。
Int J Mol Sci. 2023 Jul 11;24(14):11313. doi: 10.3390/ijms241411313.
6
Molecular and cellular mechanisms underlying the hepatoprotective role of ghrelin against NAFLD progression.ghrelin 对非酒精性脂肪性肝病进展的肝保护作用的分子和细胞机制。
J Physiol Biochem. 2023 Nov;79(4):833-849. doi: 10.1007/s13105-022-00933-1. Epub 2022 Nov 22.
RIPK3 作为一种脂质代谢调节剂，在非酒精性脂肪性肝病中参与炎症和致癌作用。
Gut. 2021 Dec;70(12):2359-2372. doi: 10.1136/gutjnl-2020-321767. Epub 2020 Dec 24.
4
Cell Death in Liver Diseases: A Review.肝病中的细胞死亡：综述
Int J Mol Sci. 2020 Dec 18;21(24):9682. doi: 10.3390/ijms21249682.
5
A necroptotic-independent function of MLKL in regulating endothelial cell adhesion molecule expression.MLKL 在调节内皮细胞黏附分子表达中的坏死依赖功能。
Cell Death Dis. 2020 Apr 24;11(4):282. doi: 10.1038/s41419-020-2483-3.
6
Lytic cell death in metabolic liver disease.代谢性肝病中的细胞溶解性死亡
J Hepatol. 2020 Aug;73(2):394-408. doi: 10.1016/j.jhep.2020.04.001. Epub 2020 Apr 13.
7
MLKL-dependent signaling regulates autophagic flux in a murine model of non-alcohol-associated fatty liver and steatohepatitis.MLKL 依赖性信号通路调控非酒精性脂肪性肝病和脂肪性肝炎小鼠模型中的自噬流。
J Hepatol. 2020 Sep;73(3):616-627. doi: 10.1016/j.jhep.2020.03.023. Epub 2020 Mar 24.
8
Depletion of MLKL inhibits invasion of radioresistant nasopharyngeal carcinoma cells by suppressing epithelial-mesenchymal transition.敲除混合谱系激酶结构域样蛋白（MLKL）可通过抑制上皮-间质转化来抑制放射性抗性鼻咽癌细胞的侵袭。
Ann Transl Med. 2019 Dec;7(23):741. doi: 10.21037/atm.2019.11.104.
9
Inhibition of receptor-interacting protein kinase 1 improves experimental non-alcoholic fatty liver disease.抑制受体相互作用蛋白激酶1可改善实验性非酒精性脂肪性肝病。
J Hepatol. 2020 Apr;72(4):627-635. doi: 10.1016/j.jhep.2019.11.008. Epub 2019 Nov 21.
10
Necroptosis: a crucial pathogenic mediator of human disease.细胞程序性坏死：人类疾病的关键致病介质。
JCI Insight. 2019 Aug 8;4(15). doi: 10.1172/jci.insight.128834.