Noël Agnès, Jost Maud, Lambert Vincent, Lecomte Julie, Rakic Jean-Marie
Laboratory of Tumor and Development Biology, Center for Experimental Cancer Research, Center for Biomedical Integrative Genoproteomics, University of Liège, B-4000 Liège, Belgium.
Trends Mol Med. 2007 Aug;13(8):345-52. doi: 10.1016/j.molmed.2007.06.005. Epub 2007 Jul 17.
Age-related macular degeneration (AMD) is the leading cause of blindness in elderly patients. The more aggressive exudative form is characterized by abnormal blood-vessel development that occurs beneath the retina as a result of choroidal neovascularization (CNV). Vascular endothelial growth factor (VEGF) has emerged as the key mediator of CNV formation; this has led to intensive research on VEGF and the recent approval of anti-VEGF compounds by the US Food and Drug Administration. Despite this successful introduction of anti-angiogenic therapies into the clinical setting, there is still a lack of treatments that definitively reverse damaged vision. Here, we consider the importance of putative molecular targets other than VEGF that might have been underestimated. Emerging cellular mechanisms offer additional opportunities for innovative therapeutic approaches.
年龄相关性黄斑变性（AMD）是老年患者失明的主要原因。更具侵袭性的渗出性形式的特征是由于脉络膜新生血管形成（CNV），在视网膜下方发生异常血管发育。血管内皮生长因子（VEGF）已成为CNV形成的关键介质；这导致了对VEGF的深入研究以及美国食品药品监督管理局最近批准了抗VEGF化合物。尽管抗血管生成疗法已成功引入临床，但仍然缺乏能够明确逆转受损视力的治疗方法。在此，我们考虑了可能被低估的除VEGF之外的假定分子靶点的重要性。新出现的细胞机制为创新治疗方法提供了更多机会。
