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2015•Journal of Ocular Pharmacology and TherapeuticsRequires access

Thrombospondin-1 and Pathogenesis of Age-Related Macular Degeneration

Michael Housset, Florian Sennlaub

Open publisher page 19 citations

Abstract

The cardinal features of age-related macular degeneration (AMD) are the accumulation of subretinal debris, subretinal inflammation, neovascularization, and degeneration of the photoreceptors and retinal pigment epithelium (RPE). Thrombospondin-1 (TSP-1) is a major matricellular protein that is physiologically expressed in the RPE and choroid, but severely diminished in eyes with AMD. TSP-1 plays an important role in phagocytosis, potently inhibits neovascularization, and mediates immune suppression and immune privilege. The lack of TSP-1 could have a central role in the pathogenesis of AMD as it is implicated in the major pathways that seem to be deficient in the disease. We here give an overview of the major functions of TSP-1 and how it could intervene in AMD pathogenesis.

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What this paper is about

The cardinal features of age-related macular degeneration (AMD) are the accumulation of subretinal debris, subretinal inflammation, neovascularization, and degeneration of the photoreceptors and retinal pigment epithelium (RPE). Thrombospondin-1 (TSP-1) is a major matricellular protein that is physiologically expressed in the RPE and choroid, but severely diminished in eyes with AMD. TSP-1 plays an important role in phagocytosis, potently inhibits neovascularization, and mediates immune suppression and immune privilege. The lack of TSP-1 could have a central role in the pathogenesis of AMD as it is implicated in the major pathways that seem to be deficient in the disease. We here give an overview of the major functions of TSP-1 and how it could intervene in AMD pathogenesis.

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OpenAlex reports 19 citations for this work. Citation counts describe recorded attention and do not establish research quality.

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Available abstract

The cardinal features of age-related macular degeneration (AMD) are the accumulation of subretinal debris, subretinal inflammation, neovascularization, and degeneration of the photoreceptors and retinal pigment epithelium (RPE). Thrombospondin-1 (TSP-1) is a major matricellular protein that is physiologically expressed in the RPE and choroid, but severely diminished in eyes with AMD. TSP-1 plays an important role in phagocytosis, potently inhibits neovascularization, and mediates immune suppression and immune privilege. The lack of TSP-1 could have a central role in the pathogenesis of AMD as it is implicated in the major pathways that seem to be deficient in the disease. We here give an overview of the major functions of TSP-1 and how it could intervene in AMD pathogenesis.

Key concepts: Macular degeneration, Pathogenesis, Drusen, Immune privilege, Retinal pigment epithelium, Matricellular protein, ABCA4, Choroidal neovascularization

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