The emerging role of cuproptosis in spinal cord injury

Copper is a vital trace element integral to numerous biological processes, including iron metabolism, neurotransmitter synthesis, mitochondrial respiration, oxidative stress regulation, and energy production. However, disturbances in copper metabolism can result in pathological conditions, including...

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Main Authors: Daoran Xu, Liyu Hu, Jinming Zhou, Xiongwei Deng, Yunrong Zhu, Chao Liu
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-06-01
Series:Frontiers in Immunology
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Online Access:https://www.frontiersin.org/articles/10.3389/fimmu.2025.1595852/full
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author Daoran Xu
Liyu Hu
Jinming Zhou
Xiongwei Deng
Yunrong Zhu
Chao Liu
author_facet Daoran Xu
Liyu Hu
Jinming Zhou
Xiongwei Deng
Yunrong Zhu
Chao Liu
author_sort Daoran Xu
collection DOAJ
description Copper is a vital trace element integral to numerous biological processes, including iron metabolism, neurotransmitter synthesis, mitochondrial respiration, oxidative stress regulation, and energy production. However, disturbances in copper metabolism can result in pathological conditions, including cuproptosis—a newly recognized form of programmed cell death (PCD) marked by copper accumulation and the disruption of copper-dependent metabolic pathways. Cuproptosis has been associated with various diseases, such as cancer, metabolic disorders and neurodegenerative disorders. In the context of spinal cord injury (SCI), multiple pathological mechanisms, including oxidative stress, inflammation, and PCD could impact the patient’s prognosis with SCI. This review seeks to elucidate the pathophysiological underpinnings of SCI, the mechanisms and biological significance of copper homeostasis and the role of cuproptosis in SCI.
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issn 1664-3224
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publishDate 2025-06-01
publisher Frontiers Media S.A.
record_format Article
series Frontiers in Immunology
spelling doaj-art-50eaaea1f39842e484ed76bf5a6be9252025-08-20T03:20:10ZengFrontiers Media S.A.Frontiers in Immunology1664-32242025-06-011610.3389/fimmu.2025.15958521595852The emerging role of cuproptosis in spinal cord injuryDaoran XuLiyu HuJinming ZhouXiongwei DengYunrong ZhuChao LiuCopper is a vital trace element integral to numerous biological processes, including iron metabolism, neurotransmitter synthesis, mitochondrial respiration, oxidative stress regulation, and energy production. However, disturbances in copper metabolism can result in pathological conditions, including cuproptosis—a newly recognized form of programmed cell death (PCD) marked by copper accumulation and the disruption of copper-dependent metabolic pathways. Cuproptosis has been associated with various diseases, such as cancer, metabolic disorders and neurodegenerative disorders. In the context of spinal cord injury (SCI), multiple pathological mechanisms, including oxidative stress, inflammation, and PCD could impact the patient’s prognosis with SCI. This review seeks to elucidate the pathophysiological underpinnings of SCI, the mechanisms and biological significance of copper homeostasis and the role of cuproptosis in SCI.https://www.frontiersin.org/articles/10.3389/fimmu.2025.1595852/fullspinal cord injuryreactive oxygen speciescopper homeostasiscuproptosisprogrammed cell death
spellingShingle Daoran Xu
Liyu Hu
Jinming Zhou
Xiongwei Deng
Yunrong Zhu
Chao Liu
The emerging role of cuproptosis in spinal cord injury
Frontiers in Immunology
spinal cord injury
reactive oxygen species
copper homeostasis
cuproptosis
programmed cell death
title The emerging role of cuproptosis in spinal cord injury
title_full The emerging role of cuproptosis in spinal cord injury
title_fullStr The emerging role of cuproptosis in spinal cord injury
title_full_unstemmed The emerging role of cuproptosis in spinal cord injury
title_short The emerging role of cuproptosis in spinal cord injury
title_sort emerging role of cuproptosis in spinal cord injury
topic spinal cord injury
reactive oxygen species
copper homeostasis
cuproptosis
programmed cell death
url https://www.frontiersin.org/articles/10.3389/fimmu.2025.1595852/full
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