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棕榈酰化在细胞焦亡中的新作用

Emerging roles of palmitoylation in pyroptosis.

作者信息

Zhang Na, Yang Yuanxin, Xu Daichao

机构信息

Interdisciplinary Research Center on Biology and Chemistry, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai, 201210, China.

Interdisciplinary Research Center on Biology and Chemistry, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai, 201210, China; State Key Laboratory of Chemical Biology, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai, 200032, China; Shanghai Key Laboratory of Aging Studies, Shanghai, 201210, China.

出版信息

Trends Cell Biol. 2024 Nov 8. doi: 10.1016/j.tcb.2024.10.005.

DOI:10.1016/j.tcb.2024.10.005
PMID:39521664
Abstract

Pyroptosis is a lytic, proinflammatory type of programmed cell death crucial for the immune response to pathogen infections and internal danger signals. Gasdermin D (GSDMD) acts as the pore-forming protein in pyroptosis following inflammasome activation. While recent research has improved our understanding of pyroptosis activation and execution, many aspects regarding the molecular mechanisms controlling inflammasome and GSDMD activation remain to be elucidated. A growing body of literature has shown that S-palmitoylation, a reversible post-translational modification (PTM) that attaches palmitate to cysteine residues, contributes to multi-layered regulation of pyroptosis. This review summarizes the emerging roles of S-palmitoylation in pyroptosis research with a focus on mechanisms that regulate NLRP3 inflammasome and GSDMD activation.

摘要

细胞焦亡是一种溶解性、促炎性的程序性细胞死亡,对病原体感染和内部危险信号的免疫反应至关重要。在炎性小体激活后,gasdermin D(GSDMD)作为细胞焦亡中形成孔道的蛋白质发挥作用。虽然最近的研究增进了我们对细胞焦亡激活和执行的理解,但关于控制炎性小体和GSDMD激活的分子机制的许多方面仍有待阐明。越来越多的文献表明,S-棕榈酰化是一种将棕榈酸酯附着于半胱氨酸残基的可逆翻译后修饰(PTM),有助于对细胞焦亡进行多层次调节。本综述总结了S-棕榈酰化在细胞焦亡研究中的新作用,重点关注调节NLRP3炎性小体和GSDMD激活的机制。

相似文献

1
Emerging roles of palmitoylation in pyroptosis.棕榈酰化在细胞焦亡中的新作用
Trends Cell Biol. 2024 Nov 8. doi: 10.1016/j.tcb.2024.10.005.
2
Palmitoylation at a conserved cysteine residue facilitates gasdermin D-mediated pyroptosis and cytokine release.棕榈酰化在保守半胱氨酸残基上促进了 gasdermin D 介导的细胞焦亡和细胞因子释放。
Proc Natl Acad Sci U S A. 2024 Jul 16;121(29):e2400883121. doi: 10.1073/pnas.2400883121. Epub 2024 Jul 9.
3
When pyro(ptosis) meets palm(itoylation).当焦亡(ptosis)遇见棕榈酰化(itoylation)。
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ROS-dependent S-palmitoylation activates cleaved and intact gasdermin D.ROS 依赖性 S-棕榈酰化激活裂解型和完整型 gasdermin D。
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NU6300 covalently reacts with cysteine-191 of gasdermin D to block its cleavage and palmitoylation.NU6300 与 gasdermin D 的半胱氨酸 191 发生共价反应,阻止其裂解和棕榈酰化。
Sci Adv. 2024 Feb 9;10(6):eadi9284. doi: 10.1126/sciadv.adi9284. Epub 2024 Feb 7.
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Controlling pyroptosis through post-translational modifications of gasdermin D.通过对gasdermin D进行翻译后修饰来控制细胞焦亡
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Hematopoietic NLRP3 and AIM2 Inflammasomes Promote Diabetes-Accelerated Atherosclerosis, but Increased Necrosis Is Independent of Pyroptosis.造血 NLRP3 和 AIM2 炎性小体促进糖尿病加速动脉粥样硬化,但增加的坏死不依赖于细胞焦亡。
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Targeting BRD4 mitigates hepatocellular lipotoxicity by suppressing the NLRP3 inflammasome activation and GSDMD-mediated hepatocyte pyroptosis.靶向 BRD4 通过抑制 NLRP3 炎性小体激活和 GSDMD 介导热激性肝细胞细胞凋亡来减轻肝细胞脂肪毒性。
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Igniting hope: Harnessing NLRP3 inflammasome-GSDMD-mediated pyroptosis for cancer immunotherapy.点燃希望:利用 NLRP3 炎性体-GSDMD 介导的细胞焦亡进行癌症免疫治疗。
Life Sci. 2024 Oct 1;354:122951. doi: 10.1016/j.lfs.2024.122951. Epub 2024 Aug 8.

引用本文的文献

1
TLR9-Driven S-Palmitoylation in Dendritic Cells Reveals Immune and Metabolic Protein Targets.树突状细胞中TLR9驱动的S-棕榈酰化揭示免疫和代谢蛋白靶点。
Eur J Immunol. 2025 Aug;55(8):e70039. doi: 10.1002/eji.70039.
2
Protein regulatory network mediated by palmitoylation modifications in the pathological progression of Parkinson's disease: a narrative review.棕榈酰化修饰介导的蛋白质调控网络在帕金森病病理进展中的作用:一篇叙述性综述
Front Immunol. 2025 Jul 9;16:1615001. doi: 10.3389/fimmu.2025.1615001. eCollection 2025.
3
Role of S-palmitoylation in digestive system diseases.
S-棕榈酰化在消化系统疾病中的作用。
Cell Death Discov. 2025 Jul 18;11(1):331. doi: 10.1038/s41420-025-02629-z.
4
Updated insights into the molecular networks for NLRP3 inflammasome activation.对NLRP3炎性小体激活分子网络的最新见解。
Cell Mol Immunol. 2025 Apr 30. doi: 10.1038/s41423-025-01284-9.
5
Macrophage pyroptosis and its crucial role in ALI/ARDS.巨噬细胞焦亡及其在急性肺损伤/急性呼吸窘迫综合征中的关键作用。
Front Immunol. 2025 Feb 14;16:1530849. doi: 10.3389/fimmu.2025.1530849. eCollection 2025.