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微生物感染中线粒体与溶酶体的相互作用

Mitochondria-lysosome crosstalk in microbial infections.

作者信息

He Qianqian, Huang Tiantian, Chen Zhihui, Sha Zhou, Wu Haibo

机构信息

School of Life Sciences, Chongqing University, Chongqing, 401331, China.

出版信息

Sci China Life Sci. 2025 Sep 8. doi: 10.1007/s11427-024-3037-1.

DOI:10.1007/s11427-024-3037-1
PMID:40938552
Abstract

Coordination between different organelles and metabolic cues is crucial for resistance to pathogen invasion. As the core of maintaining cellular metabolism and homeostasis, mitochondria and lysosomes cooperate in the immune responses and elimination of intracellular pathogens. Previous research has focused on the function of one or the other in isolation, ignoring their pervasive interplay. In this review, we discuss the intricate mechanism of mitochondria-lysosome crosstalk and point out the role of AMP-activated protein kinase (AMPK)-transcription factor EB (TFEB) axis in microbial infections. The crosstalk between mitochondria and lysosomes affects cellular key processes, such as autophagy and programmed death, which play an important role in microbial infections.

摘要

不同细胞器与代谢信号之间的协调对于抵抗病原体入侵至关重要。作为维持细胞代谢和内稳态的核心,线粒体和溶酶体在免疫反应及清除细胞内病原体方面相互协作。以往研究多聚焦于二者各自的功能,而忽略了它们之间广泛存在的相互作用。在本综述中,我们探讨了线粒体 - 溶酶体相互作用的复杂机制,并指出AMP激活的蛋白激酶(AMPK)-转录因子EB(TFEB)轴在微生物感染中的作用。线粒体与溶酶体之间的相互作用影响细胞的关键过程,如自噬和程序性死亡,这些过程在微生物感染中发挥着重要作用。

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本文引用的文献

1
TGFB signaling induces mitophagy via PLSCR3-mediated cardiolipin externalization in conjunction with a BNIP3L/NIX-, BNIP3-, and FUNDC1-dependent mechanism.转化生长因子β(TGFB)信号传导通过磷脂 scramblase 3(PLSCR3)介导的心磷脂外化,结合 BNIP3L/NIX、BNIP3 和 FUNDC1 依赖性机制诱导线粒体自噬。
Autophagy. 2025 Apr 1:1-11. doi: 10.1080/15548627.2025.2483441.
2
TRPML1 agonist ML-SA5 mitigates uranium-induced nephrotoxicity via promoting lysosomal exocytosis.瞬时受体电位黏蛋白1激动剂ML-SA5通过促进溶酶体胞吐作用减轻铀诱导的肾毒性。
Biomed Pharmacother. 2024 Dec;181:117728. doi: 10.1016/j.biopha.2024.117728. Epub 2024 Dec 7.
3
SARS-CoV-2 NSP6 reduces autophagosome size and affects viral replication via sigma-1 receptor.
SARS-CoV-2 NSP6 通过 sigma-1 受体减少自噬体大小并影响病毒复制。
J Virol. 2024 Nov 19;98(11):e0075424. doi: 10.1128/jvi.00754-24. Epub 2024 Oct 24.
4
Quality control of mitochondria involves lysosomes in multiple definitive ways.线粒体的质量控制涉及溶酶体的多种明确方式。
Autophagy. 2024 Dec;20(12):2599-2601. doi: 10.1080/15548627.2024.2408712. Epub 2024 Oct 6.
5
Helicobacter pylori CagA mediated mitophagy to attenuate the NLRP3 inflammasome activation and enhance the survival of infected cells.幽门螺杆菌 CagA 介导的线粒体自噬减轻 NLRP3 炎性小体激活,增强感染细胞的存活。
Sci Rep. 2024 Sep 17;14(1):21648. doi: 10.1038/s41598-024-72534-5.
6
Lysosomes drive the piecemeal removal of mitochondrial inner membrane.溶酶体驱动线粒体内膜的逐步去除。
Nature. 2024 Aug;632(8027):1110-1117. doi: 10.1038/s41586-024-07835-w. Epub 2024 Aug 21.
7
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Nat Commun. 2024 Jul 26;15(1):6311. doi: 10.1038/s41467-024-50711-4.
8
inhibits nuclear translocation of TFEB, the master transcription factor for lysosomal biogenesis.抑制 TFEB 的核易位,TFEB 是溶酶体生物发生的主转录因子。
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9
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Autophagy. 2024 Sep;20(9):2000-2016. doi: 10.1080/15548627.2024.2353548. Epub 2024 May 18.