Large-Scale Quantitative Proteomics of Retinal Mitochondrial Fractions from Age-Related Macular Degeneration (AMD) Patients

Age-related macular degeneration (AMD) is the leading cause of blindness in seniors, with no effective treatment options available for most patients. AMD is characterized by the death of retinal pigment epithelium (RPE) and photoreceptors, resulting in central vision loss causing tremendous difficulties in performing daily tasks requiring visualization of fine details visualization. Dysfunction of RPE mitochondria is a critical early event involved in AMD pathogenesis, and we previously reported that maintaining normal mitochondrial functions in RPE could be a viable option for AMD treatment. We hypothesize that dysregulation of RPE mitochondrial proteome is highly relevant to the loss of RPE mitochondrial function during the transition from healthy aging to early AMD. The hypothesis was examined by quantitative proteomics using UHR-IonStar.

年龄相关性黄斑变性（Age-related macular degeneration, AMD）是老年人群失明的首要病因，目前绝大多数患者尚无有效治疗手段。AMD以视网膜色素上皮（retinal pigment epithelium, RPE）与光感受器细胞死亡为典型特征，进而引发中心视力丧失，给依赖精细视觉细节的日常活动带来极大困难。视网膜色素上皮线粒体功能异常是AMD发病机制中的关键早期事件，本团队既往研究证实，维持视网膜色素上皮线粒体的正常功能或可作为AMD治疗的潜在可行策略。本研究提出假说：在健康衰老向早期AMD进展的进程中，视网膜色素上皮线粒体蛋白质组失调与线粒体功能丧失高度相关。该假说通过采用UHR-IonStar技术的定量蛋白质组学方法得以验证。