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Molecular regulation of neuroinflammation in glaucoma: Current knowledge and the ongoing search for new treatment targets.
Prog Retin Eye Res. 2021 Aug 01 [Online ahead of print]PR

Abstract

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.

Authors+Show Affiliations

Department of Ophthalmology, Vagelos College of Physicians and Surgeons, Columbia University, Edward S. Harkness Eye Institute, New York, NY, USA. Electronic address: gt2320@cumc.columbia.edu.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

34348167

Citation

Tezel, Gülgün. "Molecular Regulation of Neuroinflammation in Glaucoma: Current Knowledge and the Ongoing Search for New Treatment Targets." Progress in Retinal and Eye Research, 2021, p. 100998.
Tezel G. Molecular regulation of neuroinflammation in glaucoma: Current knowledge and the ongoing search for new treatment targets. Prog Retin Eye Res. 2021.
Tezel, G. (2021). Molecular regulation of neuroinflammation in glaucoma: Current knowledge and the ongoing search for new treatment targets. Progress in Retinal and Eye Research, 100998. https://doi.org/10.1016/j.preteyeres.2021.100998
Tezel G. Molecular Regulation of Neuroinflammation in Glaucoma: Current Knowledge and the Ongoing Search for New Treatment Targets. Prog Retin Eye Res. 2021 Aug 1;100998. PubMed PMID: 34348167.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Molecular regulation of neuroinflammation in glaucoma: Current knowledge and the ongoing search for new treatment targets. A1 - Tezel,Gülgün, Y1 - 2021/08/01/ PY - 2021/05/27/received PY - 2021/07/23/revised PY - 2021/07/26/accepted PY - 2021/8/5/pubmed PY - 2021/8/5/medline PY - 2021/8/4/entrez KW - Glaucoma KW - Glia KW - Immunomodulation KW - Neurodegeneration KW - Neuroinflammation KW - Retinal ganglion cell SP - 100998 EP - 100998 JF - Progress in retinal and eye research JO - Prog Retin Eye Res N2 - 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. SN - 1873-1635 UR - https://www.unboundmedicine.com/medline/citation/34348167/Molecular_regulation_of_neuroinflammation_in_glaucoma:_Current_knowledge_and_the_ongoing_search_for_new_treatment_targets. L2 - https://linkinghub.elsevier.com/retrieve/pii/S1350-9462(21)00059-8 DB - PRIME DP - Unbound Medicine ER -
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