Faculty of Health Sciences, School of Pharmacy, University of Eastern Finland, 1627, 70211, Kuopio, Finland.
Cell Mol Life Sci. 2020 Mar;77(5):779-780. doi: 10.1007/s00018-019-03418-5. Epub 2020 Jan 2.
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.
预期寿命的延长导致与年龄相关的黄斑变性(AMD)的发病率不断上升,AMD 已经成为发达国家老年人视力严重丧失的主要原因。在干性 AMD 中,疾病最终导致广泛的视网膜萎缩,而湿性 AMD 的特征是由于脉络膜下的 Bruch 膜新生血管形成而导致视网膜水肿和突然视力丧失。干性 AMD 没有治疗方法,尽管玻璃体内注射抗血管内皮生长因子(VEGF)可以抑制新血管形成,但湿性 AMD 也需要新的治疗方法来阻止疾病进展,并为对现有药物没有积极反应的患者提供治疗。对疾病机制的了解是药物开发的前提,但 AMD 的多因素性质阻碍了这一进程。许多杰出的出版物已经揭示了 AMD 在细胞和分子水平上的机制,在这篇多作者综述中,我们从一些新的角度对这一主题进行了更广泛的探讨。