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Microglia in motor neuron disease: Signaling evidence from last 10 years

Motor neuron disease (MND), including amyotrophic lateral sclerosis, spinal muscular atrophy and others, involved the upper or lower motor neurons selective loss, is characterized by neurodegeneration and neuroinflammation, in conjunction with microglia. We summarized that pathways and key mediators...

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Detalles Bibliográficos
Autores principales: Wang, Min‐Jia, Kang, Lu, Wang, Yao‐Zheng, Yang, Bi‐Ru, Zhang, Chun, Lu, Yu‐Feng, Kang, Liang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9828749/
https://www.ncbi.nlm.nih.gov/pubmed/36309345
http://dx.doi.org/10.1002/dneu.22905
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author Wang, Min‐Jia
Kang, Lu
Wang, Yao‐Zheng
Yang, Bi‐Ru
Zhang, Chun
Lu, Yu‐Feng
Kang, Liang
author_facet Wang, Min‐Jia
Kang, Lu
Wang, Yao‐Zheng
Yang, Bi‐Ru
Zhang, Chun
Lu, Yu‐Feng
Kang, Liang
author_sort Wang, Min‐Jia
collection PubMed
description Motor neuron disease (MND), including amyotrophic lateral sclerosis, spinal muscular atrophy and others, involved the upper or lower motor neurons selective loss, is characterized by neurodegeneration and neuroinflammation, in conjunction with microglia. We summarized that pathways and key mediators are associated with microglia, such as fractalkine signaling, purinergic signaling, NF‐κB signaling, p38 MAPK signaling, TREM2‐APOE signaling, ROCK signaling, C1q signaling, and Ion channel, which are involved in the activation, proliferation, and inflammation of microglia. This review aims to identify the microglia‐related molecular target and explore potential treatment strategies for MND based on that target.
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spelling pubmed-98287492023-01-10 Microglia in motor neuron disease: Signaling evidence from last 10 years Wang, Min‐Jia Kang, Lu Wang, Yao‐Zheng Yang, Bi‐Ru Zhang, Chun Lu, Yu‐Feng Kang, Liang Dev Neurobiol Research Articles Motor neuron disease (MND), including amyotrophic lateral sclerosis, spinal muscular atrophy and others, involved the upper or lower motor neurons selective loss, is characterized by neurodegeneration and neuroinflammation, in conjunction with microglia. We summarized that pathways and key mediators are associated with microglia, such as fractalkine signaling, purinergic signaling, NF‐κB signaling, p38 MAPK signaling, TREM2‐APOE signaling, ROCK signaling, C1q signaling, and Ion channel, which are involved in the activation, proliferation, and inflammation of microglia. This review aims to identify the microglia‐related molecular target and explore potential treatment strategies for MND based on that target. John Wiley and Sons Inc. 2022-11-15 2022 /pmc/articles/PMC9828749/ /pubmed/36309345 http://dx.doi.org/10.1002/dneu.22905 Text en © 2022 The Authors. Developmental Neurobiology published by Wiley Periodicals LLC. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, 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 Research Articles
Wang, Min‐Jia
Kang, Lu
Wang, Yao‐Zheng
Yang, Bi‐Ru
Zhang, Chun
Lu, Yu‐Feng
Kang, Liang
Microglia in motor neuron disease: Signaling evidence from last 10 years
title Microglia in motor neuron disease: Signaling evidence from last 10 years
title_full Microglia in motor neuron disease: Signaling evidence from last 10 years
title_fullStr Microglia in motor neuron disease: Signaling evidence from last 10 years
title_full_unstemmed Microglia in motor neuron disease: Signaling evidence from last 10 years
title_short Microglia in motor neuron disease: Signaling evidence from last 10 years
title_sort microglia in motor neuron disease: signaling evidence from last 10 years
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9828749/
https://www.ncbi.nlm.nih.gov/pubmed/36309345
http://dx.doi.org/10.1002/dneu.22905
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