陈之昭

美国NIH 免疫实验室

Age-related macular degeneration (AMD) is the leading cause of blindness for older individuals. AMD pathology is characterized mainly by degeneration of photoreceptors， RPE， Bruch’s membrane， and less prominently， choroidal capillaries in the macula. Early AMD includes drusen， and advanced AMD includes geographic atrophy (‘dry’) and choroidal neovascularization (‘wet’). Currently AMD is considered a complex disease triggered by environmental factors in genetically predisposed individuals. Growing evidences have documented the key role of various inflammatory factors in the pathogenesis of AMD. Macrophages， activated microglia， and depositions of complement factors are found in AMD lesions. Molecular pathologies of inflammatory molecules， CX3CR1 and complement factor H (CFH)， and their involvements in AMD lesions reveal decreased CX3CR1 and its transcripts in AMD lesions， particularly those with risk-conferring variant of CX3CR1， and likewise， elevated C-reactive protein in the choroid of AMD eyes with risk-conferring variant of CFH. The findings validate the association between CX3CR1 or CFH polymorphism and increased risk of AMD. Moreover， the Ccl2， Ccr2， Cx3cr1， and Ccl2/Cx3cr1 deficient murine models of AMD also support these concepts. Further research is needed to determine the inflammatory mechanisms underlying the development， progression and prognosis of AMD； and to identify the specific molecules， which might be targeted the specific inflammatory elements to prevent and treat this common blindness-causing disease.

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