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Function of GSK‑3 signaling in spinal cord injury (Review)
Spinal cord injury (SCI) is a major social problem with a heavy burden on patient physiology and psychology. Glial scar formation and irreversible neuron loss are the two key points during SCI progression. During the acute phase of spinal cord injury, glial scars form, limiting the progression of in...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2023
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10587879/ https://www.ncbi.nlm.nih.gov/pubmed/37869638 http://dx.doi.org/10.3892/etm.2023.12240 |
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author | Dong, Xiong Hong, Hongxiang Cui, Zhiming |
author_facet | Dong, Xiong Hong, Hongxiang Cui, Zhiming |
author_sort | Dong, Xiong |
collection | PubMed |
description | Spinal cord injury (SCI) is a major social problem with a heavy burden on patient physiology and psychology. Glial scar formation and irreversible neuron loss are the two key points during SCI progression. During the acute phase of spinal cord injury, glial scars form, limiting the progression of inflammation. However, in the subacute or chronic phase, glial scarring inhibits axon regeneration. Following spinal cord injury, irreversible loss of neurons leads to further aggravation of spinal cord injury. Several therapies have been developed to improve either glial scar or neuron loss; however, few therapies reach the stage of clinical trials and there are no mainstream therapies for SCI. Exploring the key mechanism of SCI is crucial for finding further treatments. Glycogen synthase kinase-3 (GSK-3) is a widely expressed kinase with important physiological and pathophysiological functions in vivo. Dysfunction of the GSK-3 signaling pathway during SCI has been widely discussed for controlling neurite growth in vitro and in vivo, improving the proliferation and neuronal differentiation of endogenous neural stem cells and functional recovery from spinal cord injury. SCI can decrease the phosphorylated (p)/total (t)-GSK-3β ratio, which leads to an increase in apoptosis, whereas treatment with GSK-3 inhibitors can promote neurogenesis. In addition, several therapies for the treatment of SCI involve signaling pathways associated with GSK-3. Furthermore, signaling pathways associated with GSK-3 also participate in the pathological process of neuropathic pain that remains following SCI. The present review summarized the roles of GSK-3 signaling in SCI to aid in the understanding of GSK-3 signaling during the pathological processes of SCI and to provide evidence for the development of comprehensive treatments. |
format | Online Article Text |
id | pubmed-10587879 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-105878792023-10-21 Function of GSK‑3 signaling in spinal cord injury (Review) Dong, Xiong Hong, Hongxiang Cui, Zhiming Exp Ther Med Review Spinal cord injury (SCI) is a major social problem with a heavy burden on patient physiology and psychology. Glial scar formation and irreversible neuron loss are the two key points during SCI progression. During the acute phase of spinal cord injury, glial scars form, limiting the progression of inflammation. However, in the subacute or chronic phase, glial scarring inhibits axon regeneration. Following spinal cord injury, irreversible loss of neurons leads to further aggravation of spinal cord injury. Several therapies have been developed to improve either glial scar or neuron loss; however, few therapies reach the stage of clinical trials and there are no mainstream therapies for SCI. Exploring the key mechanism of SCI is crucial for finding further treatments. Glycogen synthase kinase-3 (GSK-3) is a widely expressed kinase with important physiological and pathophysiological functions in vivo. Dysfunction of the GSK-3 signaling pathway during SCI has been widely discussed for controlling neurite growth in vitro and in vivo, improving the proliferation and neuronal differentiation of endogenous neural stem cells and functional recovery from spinal cord injury. SCI can decrease the phosphorylated (p)/total (t)-GSK-3β ratio, which leads to an increase in apoptosis, whereas treatment with GSK-3 inhibitors can promote neurogenesis. In addition, several therapies for the treatment of SCI involve signaling pathways associated with GSK-3. Furthermore, signaling pathways associated with GSK-3 also participate in the pathological process of neuropathic pain that remains following SCI. The present review summarized the roles of GSK-3 signaling in SCI to aid in the understanding of GSK-3 signaling during the pathological processes of SCI and to provide evidence for the development of comprehensive treatments. D.A. Spandidos 2023-10-03 /pmc/articles/PMC10587879/ /pubmed/37869638 http://dx.doi.org/10.3892/etm.2023.12240 Text en Copyright: © Dong et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Review Dong, Xiong Hong, Hongxiang Cui, Zhiming Function of GSK‑3 signaling in spinal cord injury (Review) |
title | Function of GSK‑3 signaling in spinal cord injury (Review) |
title_full | Function of GSK‑3 signaling in spinal cord injury (Review) |
title_fullStr | Function of GSK‑3 signaling in spinal cord injury (Review) |
title_full_unstemmed | Function of GSK‑3 signaling in spinal cord injury (Review) |
title_short | Function of GSK‑3 signaling in spinal cord injury (Review) |
title_sort | function of gsk‑3 signaling in spinal cord injury (review) |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10587879/ https://www.ncbi.nlm.nih.gov/pubmed/37869638 http://dx.doi.org/10.3892/etm.2023.12240 |
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