Role of serine/arginine-rich protein kinase in the formation of choroidal neovascularization

在发达国家，年龄相关性黄斑变性（AMD）是视力丧失的主要原因。近年来的研究有力地证明了生长因子和细胞因子，如血管内皮生长因子（VEGF）在AMD的病理性血管生成、脉络膜新生血管化（CNV）过程中起着关键作用。VEGF pre-mRNA的选择性剪接受剪接调节因子的调控，包括各种富含丝氨酸/精氨酸（SR）的蛋白，这些蛋白被SR蛋白激酶（SRPK）激活。在这项研究中，我们阐明了SRPK的特异性抑制剂SRPIN340在激光诱导的CNV模型中减弱了CNV的形成。

Age-related macular degeneration (AMD) is a primary cause of visual loss in developed countries. Recent studies have provided strong evidence that growth factors and cytokines, such as vascular endothelial growth factor (VEGF), play a pivotal role in the process of pathological angiogenesis, choroidal neovascualization (CNV) in AMD. The alternative splicing of VEGF pre-mRNA is regulated by splicing regulatory factors including various serine/arginine-rich (SR) proteins, which are activated by SR protein kinase (SRPK). In this study, we elucidated that a specific inhibitor for SRPK, SRPIN340, attenuates CNV formation in laser-induced CNV model.