Thrombospondin-1 and Pathogenesis of Age-Related Macular Degeneration

被引:12
|
作者
Housset, Michael [1 ,2 ,3 ]
Sennlaub, Florian [1 ,2 ,3 ,4 ]
机构
[1] Univ Paris 06, Sorbonne Univ, Inst Vis, UMR S 968, Paris, France
[2] CNRS, UMR 7210, Paris, France
[3] INSERM, U968, Paris, France
[4] DHU ViewMaintain, INSERM DHOS CIC 1423, Ctr Hosp Natl Ophtalmol Quinze Vingts, Paris, France
基金
欧洲研究理事会; 芬兰科学院;
关键词
INDUCED MACROPHAGE APOPTOSIS; RETINAL DEGENERATION; IMMUNE PRIVILEGE; BRUCHS MEMBRANE; MOUSE MODEL; T-CELLS; ANGIOGENESIS; INFLAMMATION; ACTIVATION; EXPRESSION;
D O I
10.1089/jop.2015.0023
中图分类号
R77 [眼科学];
学科分类号
100212 ;
摘要
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.
引用
收藏
页码:406 / 412
页数:7
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