Cambridge, Massachusetts, United States
Age-related macular degeneration (AMD) is the most common cause of blindness among the elderly in the U.S. and worldwide. A hallmark of AMD and geographic atrophy (GA), the late stage of AMD, is photoreceptor and retinal pigment epithelium (RPE) cell death. Increasing evidence have indicated that chronic inflammatory events mediated by key pathways play a central role in the pathogenesis and development of AMD. However, the molecular nature of these inflammatory mechanisms remains unclear.
Research activities in the Bao lab focus on elucidating the role of inflammatory pathways in AMD pathogenesis. Our goal is to identify and characterize novel inflammatory signaling nodes and uncover novel cellular mechanisms causing degeneration of RPE, and eventually develop pathway selective modulators to treat AMD. One such signaling pathway recently focused in our lab includes nucleic acid sensing and its impact on RPE heath and degeneration. We identified the RIG-I/DDX58 RNA sensor as the major sensor for intracellular nucleic acids in RPE cells, giving new clues for the improved understanding of the mechanisms of action at the single cell level through in vivo observations. Further identify the cause of the disease could help to prevent progression of AMD by affecting earlier on disease pathology, i.e. intermediate stage of AMD.