Molecular regulation of neuroinflammation in glaucoma: Current knowledge and the ongoing search for new treatment targets.
Glaucoma
Glia
Immunomodulation
Neurodegeneration
Neuroinflammation
Retinal ganglion cell
Journal
Progress in retinal and eye research
ISSN: 1873-1635
Titre abrégé: Prog Retin Eye Res
Pays: England
ID NLM: 9431859
Informations de publication
Date de publication:
03 2022
03 2022
Historique:
received:
27
05
2021
revised:
23
07
2021
accepted:
26
07
2021
pubmed:
5
8
2021
medline:
22
4
2022
entrez:
4
8
2021
Statut:
ppublish
Résumé
Neuroinflammation relying on the inflammatory responses of glial cells has emerged as an impactful component of the multifactorial etiology of neurodegeneration in glaucoma. It has become increasingly evident that despite early adaptive and reparative features of glial responses, prolonged reactivity of the resident glia, along with the peripheral immune cells, create widespread toxicity to retinal ganglion cell (RGC) axons, somas, and synapses. As much as the synchronized responses of astrocytes and microglia to glaucoma-related stress or neuron injury, their bi-directional interactions are critical to build and amplify neuroinflammation and to dictate the neurodegenerative outcome. Although distinct molecular programs regulate somatic and axonal degeneration in glaucoma, inhibition of neurodegenerative inflammation can provide a broadly beneficial treatment strategy to rescue RGC integrity and function. Since inflammatory toxicity and mitochondrial dysfunction are converging etiological paths that can boost each other and feed into a vicious cycle, anti-inflammatory treatments may also offer a multi-target potential. This review presents an overview of the current knowledge on neuroinflammation in glaucoma with particular emphasis on the cell-intrinsic and cell-extrinsic factors involved in the reciprocal regulation of glial responses, the interdependence between inflammatory and mitochondrial routes of neurodegeneration, and the research aspects inspiring for prospective immunomodulatory treatments. With the advent of powerful technologies, ongoing research on molecular and functional characteristics of glial responses is expected to accumulate more comprehensive and complementary information and to rapidly move the field forward to safe and effective modulation of the glial pro-inflammatory activities, while restoring or augmenting the glial immune-regulatory and neurosupport functions.
Identifiants
pubmed: 34348167
pii: S1350-9462(21)00059-8
doi: 10.1016/j.preteyeres.2021.100998
pmc: PMC8803988
mid: NIHMS1731743
pii:
doi:
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
100998Subventions
Organisme : NEI NIH HHS
ID : P30 EY019007
Pays : United States
Organisme : NEI NIH HHS
ID : R01 EY028153
Pays : United States
Informations de copyright
Copyright © 2021 The Author. Published by Elsevier Ltd.. All rights reserved.
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