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Thrombospondin-1 and Pathogenesis of Age-Related Macular Degeneration.

Authors
  • Housset, Michael1, 2, 3
  • Sennlaub, Florian1, 2, 3, 4
  • 1 1 Sorbonne Universités , UPMC Univ Paris 06, UMR_S 968, Institut de la Vision, Paris, France . , (France)
  • 2 2 CNRS , UMR_7210, Paris, France . , (France)
  • 3 3 INSERM , U968, Paris, France . , (France)
  • 4 4 Centre Hospitalier National d'Ophtalmologie des Quinze-Vingts, DHU ViewMaintain, INSERM-DHOS CIC 1423 , Paris, France . , (France)
Type
Published Article
Journal
Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics
Publication Date
Sep 01, 2015
Volume
31
Issue
7
Pages
406–412
Identifiers
DOI: 10.1089/jop.2015.0023
PMID: 26062001
Source
Medline
License
Unknown

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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