Inflammatory pathways in pathological neovascularization in retina and choroid: A narrative review on the inflammatory drug target molecules in retinal and choroidal neovascularization

Abstract

Objective: We review inflammatory drug targets in retinal and choroidal neovascularization (NV) in narrative manner. Background: Vascular remodeling and angiogenesis are processes typically associated with wound-healing mechanisms intended to minimize ischemia and maintain tissue homeostasis. In the eye, however, these actions primarily deteriorate tissue homeostatic recovery, and could even contribute to the progress of severe conditions, e.g., blindness. Angiogenesis in diabetic retinopathy (DR) and age-related macular degeneration (AMD) is the primary cause of vision loss in working-age and elderly populations. Current treatment of anti-vascular endothelial growth factor (VEGF) agents has limited action efficacy, working in less than 50% patients. Understanding cellular and molecular networks associated in retinal vascular remodeling may provide an insight to develop novel therapeutic strategies. Methods: Here, we highlight ocular cells—endothelial, mural, retinal pigment epithelium (RPE), glial and macrophages, as well as inflammatory molecules—such as the complement system, stromal derived factor-1, chemokine CXC receptor-4, inflammasome, interleukin-18, programed cell death ligand-1, insulin-like growth factor (IGF) and sphigosin-1-phosphate receptor, associated with retinal and choroidal NV, and discuss their recent and future therapeutic approaches. Conclusions: A deeper understanding on pathogenesis, pathobiology including ocular immunobiology of retinal and choroidal NV will pave the way to expand and overleap the current therapeutic approach.