Molecular mechanisms of retinal pigment epithelium damage and development of age-related macular degeneration

被引:167
作者
Kinnunen, Kati [1 ,2 ]
Petrovski, Goran [3 ,4 ]
Moe, Morten C. [5 ]
Berta, Andras [4 ]
Kaarniranta, Kai [1 ,2 ]
机构
[1] Univ Eastern Finland, Dept Ophthalmol, Inst Clin Med, FIN-70211 Kuopio, Finland
[2] Kuopio Univ Hosp, Dept Ophthalmol, SF-70210 Kuopio, Finland
[3] Univ Debrecen, Dept Biochem & Mol Biol, Apoptosis & Genom Res Grp, Hungarian Acad Sci, H-4012 Debrecen, Hungary
[4] Univ Debrecen, Dept Ophthalmol, Med & Hlth Sci Ctr, H-4012 Debrecen, Hungary
[5] Univ Oslo, Ctr Eye Res, Dept Ophthalmol, Oslo Univ Hosp, Oslo, Norway
关键词
drusen; lipofuscin; macular degeneration; retinal pigment epithelium; ENDOTHELIAL GROWTH-FACTOR; COMPLEMENT FACTOR-H; FUNDUS AUTOFLUORESCENCE PATTERNS; ENDOPLASMIC-RETICULUM STRESS; HTRA1 PROMOTER POLYMORPHISM; GLYCATION END-PRODUCTS; BRUCHS MEMBRANE; APOLIPOPROTEIN-E; SEQUESTOSOME; 1/P62; VARIANT INCREASES;
D O I
10.1111/j.1755-3768.2011.02179.x
中图分类号
R77 [眼科学];
学科分类号
100212 ;
摘要
Age-related macular degeneration (AMD) is attributed to a complex interaction of genetic and environmental factors. It is characterized by degeneration involving the retinal photoreceptors, retinal pigment epithelium (RPE) and Bruch's membrane, as well as alterations in choroidal capillaries. AMD pathogenesis is strongly associated with chronic oxidative stress and inflammation that ultimately lead to protein damage, aggregation and degeneration of RPE. Specific degenerative findings for AMD are accumulation of intracellular lysosomal lipofuscin and extracellular drusens. In this review, we discuss thoroughly RPE-derived mechanisms in AMD pathology.
引用
收藏
页码:299 / 309
页数:11
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