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Astrocyte polarization in glaucoma: a new opportunity
Astrocyte polarization is a new concept which is similar to microglia polarization and in which astrocytes are classified as A1 (neurotoxic) and A2 (neuroprotective). Several studies on astrocyte polarization have focused mainly on neurodegenerative diseases, trauma, and infections. However, the rol...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Wolters Kluwer - Medknow
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9165360/ https://www.ncbi.nlm.nih.gov/pubmed/35662185 http://dx.doi.org/10.4103/1673-5374.339470 |
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author | Liu, Yi-Xin Sun, Hao Guo, Wen-Yi |
author_facet | Liu, Yi-Xin Sun, Hao Guo, Wen-Yi |
author_sort | Liu, Yi-Xin |
collection | PubMed |
description | Astrocyte polarization is a new concept which is similar to microglia polarization and in which astrocytes are classified as A1 (neurotoxic) and A2 (neuroprotective). Several studies on astrocyte polarization have focused mainly on neurodegenerative diseases, trauma, and infections. However, the role of astrocyte polarization in glaucoma, a neurodegenerative disease, has not been fully explored. In this review, we first describe the characteristics of astrocyte astrogliosis in glaucoma, including morphological, molecular, proliferative and functional changes. We then summarize understanding of astrocyte polarization in other diseases, and show that A1 astrocytes are involved in the death of retinal ganglion cells in glaucoma, and that their neurotoxins kill only damaged retinal ganglion cells. Based on this, we propose new interesting conjecture on astrocyte polarization in glaucoma: (1) That the neurotoxin from A1 astrocytes is a product of the complement system (membrane-attacking complex), since this system is known to mediate synaptic elimination and the C3 expression is clearly increased in A1 astrocytes; (2) that reactive scar-forming astrocytes in the optic nerve head may be classified as A2 astrocytes since their ablation leads to a worse prognosis in glaucoma. Finally, current therapeutic research progress on astrocyte polarization in other diseases is also addressed. Regulation of astrocyte polarization can be achieved by extracellular microglia-related and intracellular pathways. Reduced A1 or increased A2 astrocytes can rescue the nerve. For example, glucagon-like peptide-1 receptor agonist rescues retinal ganglion cells by reducing A1 astrocytes via the extracellular microglia-related pathway in an ocular hypertension model, suggesting that regulation of astrocyte polarization as a therapeutic target in glaucoma is feasible. |
format | Online Article Text |
id | pubmed-9165360 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Wolters Kluwer - Medknow |
record_format | MEDLINE/PubMed |
spelling | pubmed-91653602022-06-05 Astrocyte polarization in glaucoma: a new opportunity Liu, Yi-Xin Sun, Hao Guo, Wen-Yi Neural Regen Res Review Astrocyte polarization is a new concept which is similar to microglia polarization and in which astrocytes are classified as A1 (neurotoxic) and A2 (neuroprotective). Several studies on astrocyte polarization have focused mainly on neurodegenerative diseases, trauma, and infections. However, the role of astrocyte polarization in glaucoma, a neurodegenerative disease, has not been fully explored. In this review, we first describe the characteristics of astrocyte astrogliosis in glaucoma, including morphological, molecular, proliferative and functional changes. We then summarize understanding of astrocyte polarization in other diseases, and show that A1 astrocytes are involved in the death of retinal ganglion cells in glaucoma, and that their neurotoxins kill only damaged retinal ganglion cells. Based on this, we propose new interesting conjecture on astrocyte polarization in glaucoma: (1) That the neurotoxin from A1 astrocytes is a product of the complement system (membrane-attacking complex), since this system is known to mediate synaptic elimination and the C3 expression is clearly increased in A1 astrocytes; (2) that reactive scar-forming astrocytes in the optic nerve head may be classified as A2 astrocytes since their ablation leads to a worse prognosis in glaucoma. Finally, current therapeutic research progress on astrocyte polarization in other diseases is also addressed. Regulation of astrocyte polarization can be achieved by extracellular microglia-related and intracellular pathways. Reduced A1 or increased A2 astrocytes can rescue the nerve. For example, glucagon-like peptide-1 receptor agonist rescues retinal ganglion cells by reducing A1 astrocytes via the extracellular microglia-related pathway in an ocular hypertension model, suggesting that regulation of astrocyte polarization as a therapeutic target in glaucoma is feasible. Wolters Kluwer - Medknow 2022-04-29 /pmc/articles/PMC9165360/ /pubmed/35662185 http://dx.doi.org/10.4103/1673-5374.339470 Text en Copyright: © Neural Regeneration Research https://creativecommons.org/licenses/by-nc-sa/4.0/This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms. |
spellingShingle | Review Liu, Yi-Xin Sun, Hao Guo, Wen-Yi Astrocyte polarization in glaucoma: a new opportunity |
title | Astrocyte polarization in glaucoma: a new opportunity |
title_full | Astrocyte polarization in glaucoma: a new opportunity |
title_fullStr | Astrocyte polarization in glaucoma: a new opportunity |
title_full_unstemmed | Astrocyte polarization in glaucoma: a new opportunity |
title_short | Astrocyte polarization in glaucoma: a new opportunity |
title_sort | astrocyte polarization in glaucoma: a new opportunity |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9165360/ https://www.ncbi.nlm.nih.gov/pubmed/35662185 http://dx.doi.org/10.4103/1673-5374.339470 |
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