Complement activation, lipid metabolism, and mitochondrial injury: Converging pathways in age-related macular degeneration

Complement activation, lipid metabolism, and mitochondrial injury: Converging pathways in age-related macular degeneration

Blog Article

The retinal pigment epithelium (RPE) is the primary site of injury in non-neovascular vector gp68hx 12vh-012ca age-related macular degeneration or dry AMD.Polymorphisms in genes that regulate complement activation and cholesterol metabolism are strongly associated with AMD, but the biology underlying disease-associated variants is not well understood.Here, we highlight recent studies that have used molecular, biochemical, and live-cell imaging methods to elucidate mechanisms by which aging-associated insults conspire with AMD genetic risk variants to tip the balance towards disease.We discuss how critical functions including lipid metabolism, autophagy, complement regulation, and mitochondrial dynamics are compromised gu502lv-bi7n8 in the RPE, and how a deeper understanding of these mechanisms has helped identify promising therapeutic targets to preserve RPE homeostasis in AMD.