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Multifactorial Pathogenic Processes of Retinal Ganglion Cell Degeneration in Glaucoma towards Multi-Target Strategies for Broader Treatment Effects.
Cells. 2021 06 02; 10(6)C

Abstract

Glaucoma is a chronic neurodegenerative disease characterized by apoptosis of retinal ganglion cell (RGC) somas, degeneration of axons, and loss of synapses at dendrites and axon terminals. Glaucomatous neurodegeneration encompasses multiple triggers, multiple cell types, and multiple molecular pathways through the etiological paths with biomechanical, vascular, metabolic, oxidative, and inflammatory components. As much as intrinsic responses of RGCs themselves, divergent responses and intricate interactions of the surrounding glia also play decisive roles for the cell fate. Seen from a broad perspective, multitarget treatment strategies have a compelling pathophysiological basis to more efficiently manipulate multiple pathogenic processes at multiple injury sites in such a multifactorial neurodegenerative disease. Despite distinct molecular programs for somatic and axonal degeneration, mitochondrial dysfunction and glia-driven neuroinflammation present interdependent processes with widespread impacts in the glaucomatous retina and optic nerve. Since dysfunctional mitochondria stimulate inflammatory responses and proinflammatory mediators impair mitochondria, mitochondrial restoration may be immunomodulatory, while anti-inflammatory treatments protect mitochondria. Manipulation of these converging routes may thus allow a unified treatment strategy to protect RGC axons, somas, and synapses. This review presents an overview of recent research advancements with emphasis on potential treatment targets to achieve the best treatment efficacy to preserve visual function in glaucoma.

Authors+Show Affiliations

Department of Ophthalmology, Vagelos College of Physicians and Surgeons, Columbia University, Edward S. Harkness Eye Institute, 635 W 165th St., Box 102, New York, NY 10032, USA.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

34199494

Citation

Tezel, Gülgün. "Multifactorial Pathogenic Processes of Retinal Ganglion Cell Degeneration in Glaucoma Towards Multi-Target Strategies for Broader Treatment Effects." Cells, vol. 10, no. 6, 2021.
Tezel G. Multifactorial Pathogenic Processes of Retinal Ganglion Cell Degeneration in Glaucoma towards Multi-Target Strategies for Broader Treatment Effects. Cells. 2021;10(6).
Tezel, G. (2021). Multifactorial Pathogenic Processes of Retinal Ganglion Cell Degeneration in Glaucoma towards Multi-Target Strategies for Broader Treatment Effects. Cells, 10(6). https://doi.org/10.3390/cells10061372
Tezel G. Multifactorial Pathogenic Processes of Retinal Ganglion Cell Degeneration in Glaucoma Towards Multi-Target Strategies for Broader Treatment Effects. Cells. 2021 06 2;10(6) PubMed PMID: 34199494.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Multifactorial Pathogenic Processes of Retinal Ganglion Cell Degeneration in Glaucoma towards Multi-Target Strategies for Broader Treatment Effects. A1 - Tezel,Gülgün, Y1 - 2021/06/02/ PY - 2021/04/19/received PY - 2021/05/14/revised PY - 2021/05/29/accepted PY - 2021/7/2/entrez PY - 2021/7/3/pubmed PY - 2021/10/30/medline KW - glaucoma KW - glia KW - immunomodulation KW - neurodegeneration KW - neuroinflammation KW - neuroprotection KW - retinal ganglion cell JF - Cells JO - Cells VL - 10 IS - 6 N2 - Glaucoma is a chronic neurodegenerative disease characterized by apoptosis of retinal ganglion cell (RGC) somas, degeneration of axons, and loss of synapses at dendrites and axon terminals. Glaucomatous neurodegeneration encompasses multiple triggers, multiple cell types, and multiple molecular pathways through the etiological paths with biomechanical, vascular, metabolic, oxidative, and inflammatory components. As much as intrinsic responses of RGCs themselves, divergent responses and intricate interactions of the surrounding glia also play decisive roles for the cell fate. Seen from a broad perspective, multitarget treatment strategies have a compelling pathophysiological basis to more efficiently manipulate multiple pathogenic processes at multiple injury sites in such a multifactorial neurodegenerative disease. Despite distinct molecular programs for somatic and axonal degeneration, mitochondrial dysfunction and glia-driven neuroinflammation present interdependent processes with widespread impacts in the glaucomatous retina and optic nerve. Since dysfunctional mitochondria stimulate inflammatory responses and proinflammatory mediators impair mitochondria, mitochondrial restoration may be immunomodulatory, while anti-inflammatory treatments protect mitochondria. Manipulation of these converging routes may thus allow a unified treatment strategy to protect RGC axons, somas, and synapses. This review presents an overview of recent research advancements with emphasis on potential treatment targets to achieve the best treatment efficacy to preserve visual function in glaucoma. SN - 2073-4409 UR - https://www.unboundmedicine.com/medline/citation/34199494/Multifactorial_Pathogenic_Processes_of_Retinal_Ganglion_Cell_Degeneration_in_Glaucoma_towards_Multi_Target_Strategies_for_Broader_Treatment_Effects_ L2 - https://www.mdpi.com/resolver?pii=cells10061372 DB - PRIME DP - Unbound Medicine ER -