Cellular and molecular pathology of age-related macular degeneration: potential role for proteoglycans

Al Gwairi, Othman, Thach, Lyna, Zheng, Wenhua, Osman, Narin and Little, Peter J. (2016) Cellular and molecular pathology of age-related macular degeneration: potential role for proteoglycans. Journal of Ophthalmology, 2016 2913612. doi:10.1155/2016/2913612


Author Al Gwairi, Othman
Thach, Lyna
Zheng, Wenhua
Osman, Narin
Little, Peter J.
Title Cellular and molecular pathology of age-related macular degeneration: potential role for proteoglycans
Journal name Journal of Ophthalmology   Check publisher's open access policy
ISSN 2090-004X
2090-0058
Publication date 2016-01-01
Year available 2016
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1155/2016/2913612
Open Access Status DOI
Volume 2016
Start page 2913612
Total pages 7
Place of publication New York, NY United States
Publisher Hindawi Publishing Corporation
Language eng
Subject 2731 Ophthalmology
Abstract Age-related macular degeneration (AMD) is a retinal disease evident after the age of 50 that damages the macula in the centre of retina. It leads to a loss of central vision with retained peripheral vision but eventual blindness occurs in many cases. The initiation site of AMD development is Bruch’s membrane (BM) where multiple changes occur including the deposition of plasma derived lipids, accumulation of extracellular debris, changes in cell morphology, and viability and the formation of drusen. AMD manifests as early and late stage; the latter involves cell proliferation and neovascularization in wet AMD. Current therapies target the later hyperproliferative and invasive wet stage whilst none target early developmental stages of AMD. In the lipid deposition disease atherosclerosis modified proteoglycans bind and retain apolipoproteins in the artery wall. Chemically modified trapped lipids are immunogenic and can initiate a chronic inflammatory process manifesting as atherosclerotic plaques and subsequent artery blockages, heart attacks, or strokes. As plasma derived lipoprotein deposits are found in BM in early AMD, it is possible that they arise by a similar process within the macula. In this review we consider aspects of the pathological processes underlying AMD with a focus on the potential role of modifications to secreted proteoglycans being a cause and therefore a target for the treatment of early AMD.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collections: HERDC Pre-Audit
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