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Crosstalk among mitophagy, pyroptosis, ferroptosis, and necroptosis in central nervous system injuries.

作者信息

Zhang Li, Hu Zhigang, Li Zhenxing, Lin Yixing

机构信息

Department of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, Jiangsu Province, China.

出版信息

Neural Regen Res. 2024 Aug 1;19(8):1660-1670. doi: 10.4103/1673-5374.389361. Epub 2023 Nov 8.


DOI:10.4103/1673-5374.389361
PMID:38103229
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10960298/
Abstract

Central nervous system injuries have a high rate of resulting in disability and mortality; however, at present, effective treatments are lacking. Programmed cell death, which is a genetically determined form of active and ordered cell death with many types, has recently attracted increasing attention due to its functions in determining the fate of cell survival. A growing number of studies have suggested that programmed cell death is involved in central nervous system injuries and plays an important role in the progression of brain damage. In this review, we provide an overview of the role of programmed cell death in central nervous system injuries, including the pathways involved in mitophagy, pyroptosis, ferroptosis, and necroptosis, and the underlying mechanisms by which mitophagy regulates pyroptosis, ferroptosis, and necroptosis. We also discuss the new direction of therapeutic strategies targeting mitophagy for the treatment of central nervous system injuries, with the aim to determine the connection between programmed cell death and central nervous system injuries and to identify new therapies to modulate programmed cell death following central nervous system injury. In conclusion, based on these properties and effects, interventions targeting programmed cell death could be developed as potential therapeutic agents for central nervous system injury patients.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb52/10960298/005f7b99c8ed/NRR-19-1660-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb52/10960298/c1fbfd853bfc/NRR-19-1660-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb52/10960298/2fbf2af93008/NRR-19-1660-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb52/10960298/f98f147a3eba/NRR-19-1660-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb52/10960298/4f8cdb7e5b7b/NRR-19-1660-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb52/10960298/ec47b4032280/NRR-19-1660-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb52/10960298/005f7b99c8ed/NRR-19-1660-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb52/10960298/c1fbfd853bfc/NRR-19-1660-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb52/10960298/2fbf2af93008/NRR-19-1660-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb52/10960298/f98f147a3eba/NRR-19-1660-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb52/10960298/4f8cdb7e5b7b/NRR-19-1660-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb52/10960298/ec47b4032280/NRR-19-1660-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb52/10960298/005f7b99c8ed/NRR-19-1660-g006.jpg

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Crosstalk among mitophagy, pyroptosis, ferroptosis, and necroptosis in central nervous system injuries.

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引用本文的文献

[1]
Microglial pyroptosis in neurological disorders: mechanistic crosstalk, metabolic triggers, and therapeutic frontiers.

Metab Brain Dis. 2025-8-29

[2]
O-GlcNAcylation Suppressed Apoptosis and Ferroptosis in Traumatic Brain Injury by Enhancing Mitophagy.

Neurochem Res. 2025-8-13

[3]
Using ML techniques to predict extubation outcomes for patients with central nervous system injuries in the Yun-Gui Plateau.

Sci Rep. 2025-5-22

[4]
TIGAR alleviates cognitive impairment in rats with chronic cerebral hypoperfusion by suppressing oxidative stress and pyroptosis.

Am J Transl Res. 2025-2-15

[5]
Evaluation of Prognostic Implication of Serum Mixed Lineage Kinase Domain-Like Protein in Acute Primary Supratentorial Intracerebral Hemorrhage: A Multicenter Prospective Cohort Study.

Brain Behav. 2025-3

[6]
Important regulatory role of mitophagy in diabetic microvascular complications.

J Transl Med. 2025-3-4

[7]
Insights on the crosstalk among different cell death mechanisms.

Cell Death Discov. 2025-2-10

[8]
Advances in the Study of Necroptosis in Vascular Dementia: Focus on Blood-Brain Barrier and Neuroinflammation.

CNS Neurosci Ther. 2025-2

[9]
Nicotinamide N-oxide Inhibits Microglial Pyroptosis by Upregulating Mitophagy and Alleviates Neural Damage in Rats after TBI.

Inflammation. 2024-10-30

[10]
Implications of Iron in Ferroptosis, Necroptosis, and Pyroptosis as Potential Players in TBI Morbidity and Mortality.

ASN Neuro. 2024

本文引用的文献

[1]
Mitophagy in intracerebral hemorrhage: a new target for therapeutic intervention.

Neural Regen Res. 2024-2

[2]
Cuproptosis illustrates tumor micro-environment features and predicts prostate cancer therapeutic sensitivity and prognosis.

Life Sci. 2023-7-15

[3]
Cuproptosis: mechanisms and links with cancers.

Mol Cancer. 2023-3-7

[4]
Copper homeostasis and cuproptosis in health and disease.

Signal Transduct Target Ther. 2022-11-23

[5]
Knowledge mapping of copper-induced cell death: A bibliometric study from 2012 to 2022.

Medicine (Baltimore). 2022-11-11

[6]
FOXO3a-dependent up-regulation of HSP90 alleviates cisplatin-induced apoptosis by activating FUNDC1-mediated mitophagy in hypoxic osteosarcoma cells.

Cell Signal. 2023-1

[7]
Docosahexaenoic Acid Alleviates Brain Damage by Promoting Mitophagy in Mice with Ischaemic Stroke.

Oxid Med Cell Longev. 2022

[8]
Mitophagy: A Potential Target for Pressure Overload-Induced Cardiac Remodelling.

Oxid Med Cell Longev. 2022

[9]
Emerging role of STING signalling in CNS injury: inflammation, autophagy, necroptosis, ferroptosis and pyroptosis.

J Neuroinflammation. 2022-10-4

[10]
Mitochondrial protein dysfunction in pathogenesis of neurological diseases.

Front Mol Neurosci. 2022-9-7

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