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

新生血管性年龄相关性黄斑变性 (C06) 中易位蛋白 (TSPO) 诱导 NADPH 氧化酶产生 ROS

• 批准号: 529571904
• 金额: --
• 依托单位: Klinik und Poliklinik für allgemeine Augenheilkunde
• 依托单位国家: 德国
• 项目类别: Collaborative Research Centres
• 资助国家: 德国
• 项目状态: 未结题
• 来源: https://gepris.dfg.de/gepris/projekt/529571904?language=en
• 关键词: Translocator; protein; TSPO; induced; ROS

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.

我们的假设是TSPO和nox1衍生的ROS是在新生血管性视网膜疾病中触发免疫反应的标记物和效应物。该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，在激光诱导的CNV模型中，详细识别和表征调节tspo诱导的小胶质细胞ROS产生的信号通路。此外，我们将确定激活的视网膜小胶质细胞产生ROS的精确靶细胞，解读tspo诱导的ROS产生对疾病结果有害影响的分子机制，并尝试调节这一机制。