Prolonged life expectancies contribute to the increasing prevalence of age-related macular degeneration (AMD) that is already the leading cause of severe vision loss among the elderly in developed countries. In dry AMD, the disease culminates into vast retinal atrophy, whereas the wet form is characterized by retinal edema and sudden vision loss due to neovascularization originating from the choroid beneath the Bruch's membrane. There is no treatment for dry AMD and despite intravitreal injections of anti-vascular endothelial growth factor (VEGF) that suppress the neovessel formation, also wet AMD needs new therapies to prevent the disease progression and to serve patients lacking of positive response to current medicines. Knowledge on disease mechanisms is a prerequisite for the drug development, which is hindered by the multifactorial nature of AMD. Numerous distinguished publications have revealed AMD mechanisms at the cellular and molecular level and in this multi-author review, we take a bit broader look at the topic with some novel aspects.

中文翻译：

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黄斑变性多作者综述的简介。

预期寿命的延长导致与年龄有关的黄斑变性（AMD）的患病率上升，而黄斑变性已经成为发达国家老年人严重视力丧失的主要原因。在干性AMD中，该疾病最终发展为巨大的视网膜萎缩，而湿性形式的特征是视网膜水肿和由于来自布鲁赫膜下脉络膜的脉络膜新生血管而导致的突然视力丧失。对于干性AMD，目前尚无治疗方法，尽管玻璃体内注射抑制新生血管形成的抗血管内皮生长因子（VEGF），但湿性AMD需要新的疗法来预防疾病进展并为对当前药物缺乏阳性反应的患者提供服务。对疾病机理的了解是药物开发的先决条件，AMD的多因素特性阻碍了这一点。许多杰出的出版物已经揭示了AMD在细胞和分子水平上的作用机制，在这一多作者的综述中，我们以一些新颖的方面对该主题进行了更广泛的研究。