Gelfand Bradley D, Ambati Jayakrishna
Department of Ophthalmology and Visual Sciences, University of Kentucky, Lexington, KY, USA; Department of Biomedical Engineering, University of Kentucky, Lexington, KY, USA; Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky, Lexington, KY, USA.
Department of Ophthalmology and Visual Sciences, University of Kentucky, Lexington, KY, USA; Department of Physiology, University of Kentucky, Lexington, KY, USA.
Trends Mol Med. 2016 Aug;22(8):656-670. doi: 10.1016/j.molmed.2016.06.009. Epub 2016 Jul 13.
Age-related macular degeneration (AMD) afflicts one out of every 40 individuals worldwide, causing irreversible central blindness in millions. The transformation of various tissue layers within the macula in the retina has led to competing conceptual models of the molecular pathways, cell types, and tissues responsible for the onset and progression of AMD. A model that has persisted for over 6 decades is the hemodynamic, or vascular theory of AMD progression, which states that vascular dysfunction of the choroid underlies AMD pathogenesis. Here, we re-evaluate this hypothesis in light of recent advances on molecular, anatomic, and hemodynamic changes underlying choroidal dysfunction in AMD. We propose an updated, detailed model of hemodynamic dysfunction as a mechanism of AMD development and progression.
年龄相关性黄斑变性（AMD）困扰着全球每40人中的1人，导致数百万人出现不可逆的中心性失明。视网膜黄斑区内各组织层的变化引发了关于AMD发病和进展的分子途径、细胞类型及组织的多种相互竞争的概念模型。一种持续了60多年的模型是AMD进展的血流动力学或血管理论，该理论认为脉络膜血管功能障碍是AMD发病机制的基础。在此，我们根据近期关于AMD脉络膜功能障碍潜在的分子、解剖和血流动力学变化的进展，重新评估这一假说。我们提出了一个更新的、详细的血流动力学功能障碍模型，作为AMD发生和进展的一种机制。
