• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

当细胞死亡出错时:细胞凋亡和有丝分裂细胞死亡失败的炎症后果。

When cell death goes wrong: inflammatory outcomes of failed apoptosis and mitotic cell death.

机构信息

Department of Radiation Oncology (Maastro), GROW School for Oncology and Reproduction, Maastricht University Medical Centre, Maastricht, The Netherlands.

Institute of Developmental Immunology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.

出版信息

Cell Death Differ. 2023 Feb;30(2):293-303. doi: 10.1038/s41418-022-01082-0. Epub 2022 Nov 14.

DOI:10.1038/s41418-022-01082-0
PMID:36376381
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9661468/
Abstract

Apoptosis is a regulated cellular pathway that ensures that a cell dies in a structured fashion to prevent negative consequences for the tissue or the organism. Dysfunctional apoptosis is a hallmark of numerous pathologies, and treatments for various diseases are successful based on the induction of apoptosis. Under homeostatic conditions, apoptosis is a non-inflammatory event, as the activation of caspases ensures that inflammatory pathways are disabled. However, there is an increasing understanding that under specific conditions, such as caspase inhibition, apoptosis and the apoptotic machinery can be re-wired into a process which is inflammatory. In this review we discuss how the death receptor and mitochondrial pathways of apoptosis can activate inflammation. Furthermore, we will highlight how cell death due to mitotic stress might be a special case when it comes to cell death and the induction of inflammation.

摘要

细胞凋亡是一种受调控的细胞通路,可确保细胞以有序的方式死亡,从而防止组织或机体产生负面后果。细胞凋亡功能障碍是许多病理的标志,并且基于诱导细胞凋亡,各种疾病的治疗是成功的。在稳态条件下,细胞凋亡是非炎症事件,因为半胱天冬酶的激活确保了炎症途径失活。但是,人们越来越认识到,在特定条件下,例如 caspase 抑制,细胞凋亡和凋亡机制可以重新编程为炎症过程。在这篇综述中,我们讨论了凋亡的死亡受体和线粒体途径如何激活炎症。此外,我们将重点介绍有丝分裂应激引起的细胞死亡在细胞死亡和炎症诱导方面可能是一个特殊情况。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4289/9950437/23e64ba60eb1/41418_2022_1082_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4289/9950437/66ec66491773/41418_2022_1082_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4289/9950437/aa5337ca40f9/41418_2022_1082_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4289/9950437/0ae087f64a73/41418_2022_1082_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4289/9950437/23e64ba60eb1/41418_2022_1082_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4289/9950437/66ec66491773/41418_2022_1082_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4289/9950437/aa5337ca40f9/41418_2022_1082_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4289/9950437/0ae087f64a73/41418_2022_1082_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4289/9950437/23e64ba60eb1/41418_2022_1082_Fig4_HTML.jpg

相似文献

1
When cell death goes wrong: inflammatory outcomes of failed apoptosis and mitotic cell death.当细胞死亡出错时:细胞凋亡和有丝分裂细胞死亡失败的炎症后果。
Cell Death Differ. 2023 Feb;30(2):293-303. doi: 10.1038/s41418-022-01082-0. Epub 2022 Nov 14.
2
Suppression of extracellular signal-related kinase and activation of p38 MAPK are two critical events leading to caspase-8- and mitochondria-mediated cell death in phytosphingosine-treated human cancer cells.细胞外信号调节激酶的抑制和p38丝裂原活化蛋白激酶的激活是导致植物鞘氨醇处理的人类癌细胞中半胱天冬酶-8和线粒体介导的细胞死亡的两个关键事件。
J Biol Chem. 2003 Dec 12;278(50):50624-34. doi: 10.1074/jbc.M309011200. Epub 2003 Sep 30.
3
Biochemical pathways of caspase activation during apoptosis.细胞凋亡过程中半胱天冬酶激活的生化途径。
Annu Rev Cell Dev Biol. 1999;15:269-90. doi: 10.1146/annurev.cellbio.15.1.269.
4
Caspases in Cell Death, Inflammation, and Disease.细胞死亡、炎症和疾病中的胱天蛋白酶。
Immunity. 2019 Jun 18;50(6):1352-1364. doi: 10.1016/j.immuni.2019.05.020.
5
Mitochondria and cell death-associated inflammation.线粒体与细胞死亡相关的炎症。
Cell Death Differ. 2023 Feb;30(2):304-312. doi: 10.1038/s41418-022-01094-w. Epub 2022 Nov 29.
6
Cell death independent of caspases: a review.不依赖半胱天冬酶的细胞死亡:综述
Clin Cancer Res. 2005 May 1;11(9):3155-62. doi: 10.1158/1078-0432.CCR-04-2223.
7
Clostridioides difficile toxin B alone and with pro-inflammatory cytokines induces apoptosis in enteric glial cells by activating three different signalling pathways mediated by caspases, calpains and cathepsin B.艰难梭菌毒素 B 单独或与促炎细胞因子一起通过激活 caspase、钙蛋白酶和组织蛋白酶 B 介导的三种不同信号通路诱导肠胶质细胞凋亡。
Cell Mol Life Sci. 2022 Jul 22;79(8):442. doi: 10.1007/s00018-022-04459-z.
8
Staurosporine resistance in inflammatory neutrophils is associated with the inhibition of caspase- and proteasome-mediated Mcl-1 degradation.炎症性中性粒细胞中的星形孢菌素抗性与半胱天冬酶和蛋白酶体介导的Mcl-1降解的抑制有关。
J Leukoc Biol. 2016 Jan;99(1):163-74. doi: 10.1189/jlb.3A1114-537RR. Epub 2015 Aug 26.
9
Release of mitochondrial cytochrome C in both apoptosis and necrosis induced by beta-lapachone in human carcinoma cells.β-拉帕醌诱导人癌细胞凋亡和坏死过程中线粒体细胞色素C的释放。
Mol Med. 1999 Apr;5(4):232-9.
10
Apoptosis: a mitochondrial perspective on cell death.细胞凋亡:从线粒体角度看细胞死亡
Indian J Exp Biol. 2005 Jan;43(1):25-34.

引用本文的文献

1
Comprehensive analysis of regulated cell death pathways: intrinsic disorder, protein-protein interactions, and cross-pathway communication.细胞程序性死亡途径的综合分析:内在无序、蛋白质-蛋白质相互作用及跨途径通讯
Apoptosis. 2025 Aug 19. doi: 10.1007/s10495-025-02161-6.
2
Integrated transcriptomic and immune enzymatic analyses uncover coordinated immunometabolic responses in large yellow croaker () to sp. infection.综合转录组学和免疫酶分析揭示了大黄鱼对 感染的协同免疫代谢反应。 (注:原文中“sp.”处可能有信息缺失未明确具体物种)
Front Immunol. 2025 Jul 16;16:1636453. doi: 10.3389/fimmu.2025.1636453. eCollection 2025.
3
PKM2 apoptotic vesicle-mediated systemic senolytics ameliorate chronic periodontitis.

本文引用的文献

1
Mitochondrial dynamics regulate genome stability via control of caspase-dependent DNA damage.线粒体动力学通过控制半胱天冬酶依赖性 DNA 损伤来调节基因组稳定性。
Dev Cell. 2022 May 23;57(10):1211-1225.e6. doi: 10.1016/j.devcel.2022.03.019. Epub 2022 Apr 20.
2
Immunogenic cell stress and death.免疫原性细胞应激和死亡。
Nat Immunol. 2022 Apr;23(4):487-500. doi: 10.1038/s41590-022-01132-2. Epub 2022 Feb 10.
3
The interplay between BAX and BAK tunes apoptotic pore growth to control mitochondrial-DNA-mediated inflammation.BAX 和 BAK 之间的相互作用调节凋亡孔的生长,以控制线粒体 DNA 介导的炎症。
丙酮酸激酶M2凋亡小泡介导的全身衰老细胞溶解疗法可改善慢性牙周炎。
Bioact Mater. 2025 Jul 4;51:962-976. doi: 10.1016/j.bioactmat.2025.06.041. eCollection 2025 Sep.
4
Interaction between Perivascular and Luminal Factors in Arteriovenous Fistula in Yucatan Miniswine.尤卡坦小型猪动静脉瘘中血管周围因素与管腔因素之间的相互作用
Cardiol Cardiovasc Med. 2025;9(2):82-88. Epub 2025 Mar 11.
5
PANoptosis as a Two-Edged Sword in Colorectal Cancer: A Pathogenic Mechanism and Therapeutic Opportunity.PANoptosis在结直肠癌中作为一把双刃剑:一种致病机制和治疗机遇
Cells. 2025 May 16;14(10):730. doi: 10.3390/cells14100730.
6
A morphology and secretome map of pyroptosis.细胞焦亡的形态学和分泌组图谱。
Mol Biol Cell. 2025 Jun 1;36(6):ar63. doi: 10.1091/mbc.E25-03-0119. Epub 2025 Apr 9.
7
Analysis of human brain RNA-seq data reveals combined effects of 4 types of RNA modifications and 18 types of programmed cell death on Alzheimer's disease.对人类大脑RNA测序数据的分析揭示了4种RNA修饰和18种程序性细胞死亡对阿尔茨海默病的联合作用。
J Transl Med. 2025 Apr 3;23(1):396. doi: 10.1186/s12967-025-06324-6.
8
Advances in the study of death receptor 5.死亡受体5的研究进展
Front Pharmacol. 2025 Mar 12;16:1549808. doi: 10.3389/fphar.2025.1549808. eCollection 2025.
9
Potential Therapeutic Exploitation of G Protein-Coupled Receptor 120 (GPR120/FFAR4) Signaling in Obesity-Related Metabolic Disorders.G蛋白偶联受体120(GPR120/FFAR4)信号在肥胖相关代谢紊乱中的潜在治疗应用
Int J Mol Sci. 2025 Mar 11;26(6):2501. doi: 10.3390/ijms26062501.
10
The Mechanism by Which Estrogen Level Affects Knee Osteoarthritis Pain in Perimenopause and Non-Pharmacological Measures.雌激素水平影响围绝经期膝关节骨关节炎疼痛的机制及非药物措施
Int J Mol Sci. 2025 Mar 7;26(6):2391. doi: 10.3390/ijms26062391.
Mol Cell. 2022 Mar 3;82(5):933-949.e9. doi: 10.1016/j.molcel.2022.01.008. Epub 2022 Feb 3.
4
The cGAS-STING pathway drives type I IFN immunopathology in COVID-19.cGAS-STING 通路驱动 COVID-19 中的 I 型 IFN 免疫病理学。
Nature. 2022 Mar;603(7899):145-151. doi: 10.1038/s41586-022-04421-w. Epub 2022 Jan 19.
5
Switching a conflicted bacterial DTD-tRNA code is essential for the emergence of mitochondria.转换有冲突的细菌DTD - tRNA编码对于线粒体的出现至关重要。
Sci Adv. 2022 Jan 14;8(2):eabj7307. doi: 10.1126/sciadv.abj7307. Epub 2022 Jan 12.
6
BCL-2-family protein tBID can act as a BAX-like effector of apoptosis.BCL-2 家族蛋白 tBID 可作为细胞凋亡的 BAX 样效应因子。
EMBO J. 2022 Dec 17;41(2):e108690. doi: 10.15252/embj.2021108690. Epub 2021 Dec 21.
7
TNF leads to mtDNA release and cGAS/STING-dependent interferon responses that support inflammatory arthritis.TNF 导致线粒体 DNA 释放和 cGAS/STING 依赖性干扰素反应,从而支持炎症性关节炎。
Cell Rep. 2021 Nov 9;37(6):109977. doi: 10.1016/j.celrep.2021.109977.
8
TRAIL signaling promotes entosis in colorectal cancer.TRAIL 信号促进结直肠癌的侵入。
J Cell Biol. 2021 Nov 1;220(11). doi: 10.1083/jcb.202010030. Epub 2021 Sep 21.
9
Environmental allergens trigger type 2 inflammation through ripoptosome activation.环境过敏原通过激活 ripoptosome 引发 2 型炎症。
Nat Immunol. 2021 Oct;22(10):1316-1326. doi: 10.1038/s41590-021-01011-2. Epub 2021 Sep 16.
10
Cell cycle control in cancer.癌症中的细胞周期调控。
Nat Rev Mol Cell Biol. 2022 Jan;23(1):74-88. doi: 10.1038/s41580-021-00404-3. Epub 2021 Sep 10.