Translocator protein (TSPO)-induced ROS production by NADPH oxidases in neovascular age-related macular degeneration (C06)

我们的假设是TSPO和NOX1衍生的ROS是在新生血管视网膜疾病中触发免疫反应的标志物和效应物。这个项目的总体目标是增加我们对TSPO/NOX轴如何驱动视网膜炎症性疾病(如AMD)的理解。为了解决这一问题，我们将利用转录组学和磷酸化蛋白质组学的方法，对激光诱导的CNV模型中调节TSPO诱导的小胶质细胞产生ROS的信号通路进行详细的鉴定和表征。此外，我们还将确定由激活的视网膜小胶质细胞产生的ROS的精确靶细胞，破译TSPO诱导的ROS产生对疾病转归有害影响的分子机制，并试图对其进行调节。

Our hypothesis is that TSPO and NOX1-derived ROS are markers and effectors that trigger immune responses in neovascular retinal diseases. The overall goal of this project is to increase our understanding of how the TSPO/NOX axis drives retinal inflammatory diseases, such as AMD. To address this, we will identify and characterize in detail the signaling pathways regulating TSPO-induced ROS production by microglia in the laser-induced CNV model using transcriptomics and phosphoproteomics. In addition, we will identify the precise target cells of ROS produced by activated retinal microglia, decipher the molecular mechanisms underlying the detrimental effects of TSPO-induced ROS production on disease outcome and try to modulate that.