Petrukhin Konstantin
Columbia University, Department of Ophthalmology, Eye Institute Annex, New York, NY 10032, USA.
Expert Opin Ther Targets. 2007 May;11(5):625-39. doi: 10.1517/14728222.11.5.625.
Age-related macular degeneration (AMD) is the leading cause of blindness in developed countries. There is no effective treatment for the most prevalent atrophic (dry) form of AMD. Atrophic AMD is triggered by abnormalities in the retinal pigment epithelium (RPE) that lies beneath the photoreceptor cells and normally provides critical metabolic support to these light-sensing cells. Secondary to RPE dysfunction, macular rods and cones degenerate leading to the irreversible loss of vision. Oxidative stress, formation of drusen, accumulation of lipofuscin, local inflammation and reactive gliosis represent the pathologic processes implicated in pathogenesis of atrophic AMD. This review discusses potential target areas for small-molecule and biologic intervention, which may lead to development of new therapeutic treatments for atrophic AMD.
年龄相关性黄斑变性（AMD）是发达国家失明的主要原因。对于最常见的萎缩性（干性）AMD形式，目前尚无有效的治疗方法。萎缩性AMD是由位于光感受器细胞下方的视网膜色素上皮（RPE）异常引发的，RPE通常为这些感光细胞提供关键的代谢支持。继发于RPE功能障碍后，黄斑区的视杆细胞和视锥细胞退化，导致不可逆转的视力丧失。氧化应激、玻璃膜疣的形成、脂褐素的积累、局部炎症和反应性胶质增生是萎缩性AMD发病机制中涉及的病理过程。本综述讨论了小分子和生物干预的潜在靶点领域，这可能会促成针对萎缩性AMD的新治疗方法的开发。
