Molecular Mechanisms of Glaucoma Pathogenesis with Implications to Caveolin Adaptor Protein and Caveolin-Shp2 Axis

Title
Molecular Mechanisms of Glaucoma Pathogenesis with Implications to Caveolin Adaptor Protein and Caveolin-Shp2 Axis
Publication Date
2024-08-26
Author(s)
Abbasi, Mojdeh
Gupta, Vivek
Chitranshi, Nitin
( author )
OrcID: https://orcid.org/0000-0002-6508-9865
Email: nchitran@une.edu.au
UNE Id une-id:nchitran
Moustardas, Petros
Ranjbaran,Reza
Graham, Stuart L
Type of document
Journal Article
Language
en
Entity Type
Publication
Publisher
Buck Institute for Age Research
Place of publication
United States of America
DOI
10.14336/ad.2023.1012
UNE publication id
une:1959.11/71657
Abstract

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.

Link
Citation
Aging and disease, 15(5), p. 2051-2068
ISSN
2152-5250
Start page
2051
End page
2068
Rights
Attribution 4.0 International

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