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Molecular Mechanisms of Glaucoma Pathogenesis with Implications to Caveolin Adaptor Protein and Caveolin-Shp2 Axis
Linköping University, Department of Biomedical and Clinical Sciences, Division of Sensory Organs and Communication. Linköping University, Faculty of Medicine and Health Sciences. Macquarie Univ, Australia.
Macquarie Univ, Australia.
Macquarie Univ, Australia.
Linköping University, Department of Biomedical and Clinical Sciences, Division of Sensory Organs and Communication. Linköping University, Faculty of Medicine and Health Sciences.ORCID iD: 0000-0003-3192-3708
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2024 (English)In: Aging and Disease, ISSN 2152-5250, Vol. 15, no 5, p. 2051-2068Article, review/survey (Refereed) Published
Abstract [en]

Glaucoma is a common retinal disorder characterized by progressive optic nerve damage, resulting in visual impairment and potential blindness. Elevated intraocular pressure (IOP) is a major risk factor, but some patients still experience disease progression despite IOP-lowering treatments. Genome-wide association studies have linked variations in the Caveolin1/2 (CAV-1/2) gene loci to glaucoma risk. Cav-1, a key protein in caveolae membrane invaginations, is involved in signaling pathways and its absence impairs retinal function. Recent research suggests that Cav-1 is implicated in modulating the BDNF/TrkB signaling pathway in retinal ganglion cells, which plays a critical role in retinal ganglion cell (RGC) health and protection against apoptosis. Understanding the interplay between these proteins could shed light on glaucoma pathogenesis and provide potential therapeutic targets.

Place, publisher, year, edition, pages
INT SOC AGING & DISEASE , 2024. Vol. 15, no 5, p. 2051-2068
Keywords [en]
retina; glaucoma; Caveolin; Shp2 phosphatase; IOP; RGCs
National Category
Geriatrics
Identifiers
URN: urn:nbn:se:liu:diva-199441DOI: 10.14336/AD.2023.1012ISI: 001098808600001PubMedID: 37962455OAI: oai:DiVA.org:liu-199441DiVA, id: diva2:1816998
Available from: 2023-12-05 Created: 2023-12-05 Last updated: 2024-10-22Bibliographically approved

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Abbasi, MojdehMoustardas, Petros

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