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解析分子关联:线粒体途径及其在细胞死亡串扰中的作用的深入综述。

Deciphering the Molecular Nexus: An In-Depth Review of Mitochondrial Pathways and Their Role in Cell Death Crosstalk.

机构信息

Beijing Laboratory for Separation and Analysis in Biomedicine and Pharmaceuticals, School of Medical Technology, Beijing Institute of Technology, Beijing 100081, China.

出版信息

Cells. 2024 May 17;13(10):863. doi: 10.3390/cells13100863.


DOI:10.3390/cells13100863
PMID:38786088
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11119937/
Abstract

Cellular demise is a pivotal event in both developmental processes and disease states, with mitochondrial regulation playing an essential role. Traditionally, cell death was categorized into distinct types, considered to be linear and mutually exclusive pathways. However, the current understanding has evolved to recognize the complex and interconnected mechanisms of cell death, especially within apoptosis, pyroptosis, and necroptosis. Apoptosis, pyroptosis, and necroptosis are governed by intricate molecular pathways, with mitochondria acting as central decision-makers in steering cells towards either apoptosis or pyroptosis through various mediators. The choice between apoptosis and necroptosis is often determined by mitochondrial signaling and is orchestrated by specific proteins. The molecular dialogue and the regulatory influence of mitochondria within these cell death pathways are critical research areas. Comprehending the shared elements and the interplay between these death modalities is crucial for unraveling the complexities of cellular demise.

摘要

细胞死亡是发育过程和疾病状态中的一个关键事件,线粒体调节起着至关重要的作用。传统上,细胞死亡被分为不同的类型,被认为是线性的和相互排斥的途径。然而,目前的认识已经发展到认识细胞死亡的复杂和相互关联的机制,特别是在细胞凋亡、细胞焦亡和细胞坏死中。细胞凋亡、细胞焦亡和细胞坏死受到复杂的分子途径的控制,线粒体作为中央决策者,通过各种介质引导细胞走向凋亡或细胞焦亡。凋亡和坏死的选择通常取决于线粒体信号,并由特定的蛋白质来协调。在这些细胞死亡途径中,分子对话和线粒体的调节影响是关键的研究领域。理解这些死亡方式之间的共同元素和相互作用对于揭示细胞死亡的复杂性至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85d5/11119937/b9f41ecdc5b4/cells-13-00863-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85d5/11119937/5c5e7e413f6b/cells-13-00863-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85d5/11119937/ba76f179d88f/cells-13-00863-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85d5/11119937/da00a28a6039/cells-13-00863-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85d5/11119937/b9f41ecdc5b4/cells-13-00863-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85d5/11119937/5c5e7e413f6b/cells-13-00863-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85d5/11119937/ba76f179d88f/cells-13-00863-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85d5/11119937/da00a28a6039/cells-13-00863-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85d5/11119937/b9f41ecdc5b4/cells-13-00863-g004.jpg

相似文献

[1]
Deciphering the Molecular Nexus: An In-Depth Review of Mitochondrial Pathways and Their Role in Cell Death Crosstalk.

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引用本文的文献

[1]
Targeting Cancer Cell Fate: Apoptosis, Autophagy, and Gold Nanoparticles in Treatment Strategies.

Curr Issues Mol Biol. 2025-6-14

[2]
The interplay between α-synuclein aggregation and necroptosis in Parkinson's disease: a spatiotemporal perspective.

Front Neurosci. 2025-4-8

[3]
Targeting Mitochondrial Dysfunction in Cerebral Ischemia: Advances in Pharmacological Interventions.

Antioxidants (Basel). 2025-1-18

[4]
Voltage-dependent anion channel 1 oligomerization regulates PANoptosis in retinal ischemia-reperfusion injury.

Neural Regen Res. 2025-1-13

本文引用的文献

[1]
Mitochondria-associated programmed cell death as a therapeutic target for age-related disease.

Exp Mol Med. 2023-8

[2]
Mannose antagonizes GSDME-mediated pyroptosis through AMPK activated by metabolite GlcNAc-6P.

Cell Res. 2023-12

[3]
Cloning, expression of porcine GSDME and identification of its site cleaved by caspase-3.

Biochem Biophys Res Commun. 2023-8-20

[4]
p53 regulates the mitochondrial immune checkpoint.

Trends Immunol. 2023-4

[5]
50 years on and still very much alive: 'Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics'.

Br J Cancer. 2023-2

[6]
Roles of RIPK3 in necroptosis, cell signaling, and disease.

Exp Mol Med. 2022-10

[7]
The emerging role of pyroptosis in pediatric cancers: from mechanism to therapy.

J Hematol Oncol. 2022-10-8

[8]
The resurrection of RIP kinase 1 as an early cell death checkpoint regulator-a potential target for therapy in the necroptosis era.

Exp Mol Med. 2022-9

[9]
Programmed Cell Death Tunes Tumor Immunity.

Front Immunol. 2022

[10]
Programming inflammatory cell death for therapy.

Pharmacol Ther. 2022-4

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