Fibrogliosis in neovascular age-related macular degeneration: A new mechanistic perspective

Abstract

Age-related macular degeneration (AMD) remains among the leading causes of blindness in industrialized nations, with fibrosis secondary to macular neovascularization (MNV) significantly contributing to visual decline despite treatment with anti-vascular endothelial growth factor therapy. Although traditionally viewed as detrimental, fibrosis may reflect a delicate balance between beneficial vessel stabilization and harmful scarring. We critically evaluate the pathophysiology of fibrosis in AMD and introduces the novel hypothetical concept of "fibrogliosis", which emphasizes the central role of Müller glia and retinal microglia activation following disruption of the outer blood-retinal barrier. According to this concept, fibrogliosis manifests differently among MNV subtypes, influenced largely by their impact on outer blood-retinal barrier integrity. Recognizing this variability underscores the importance of further investigation into the hypothetical concept of fibrogliosis, which in theory could guide future therapeutic strategies to balance vascular stabilization with the modulation of neovascularization and fibrosis.

Keywords: Age-related macular degeneration (AMD); Anti-VEGF; Choroidal Neovascularization (CNV); Disciform scar; Fibrogliosis; Fibrosis; Glial cells; Macular Neovascularization (MNV); Retina.