The impact of NF-κB on inflammatory and angiogenic processes in age-related macular degeneration

Age-related macular degeneration (AMD) is a prominent cause of vision loss, characterized by two different types, dry (atrophic) and wet (neovascular). Dry AMD is distinguished by the progressive deterioration of retinal cells, which ultimately causes a decline in vision. In contrast, wet AMD is defined by the abnormal development of blood vessels underneath the retina, leading to a sudden and severe vision impairment. The course of AMD is primarily driven by chronic inflammation and pathological angiogenesis, in which the NF-κB signaling pathway plays a crucial role. The activation of NF-κB results in the generation of pro-inflammatory cytokines, chemokines, and angiogenic factors like VEGF, which contribute to inflammation and the formation of new blood vessels in AMD. This review analyzes the intricate relationship between NF-κB signaling, inflammation, and angiogenesis in AMD and assesses the possibility of using NF-κB as a target for therapy. The evaluation involves a comprehensive examination of preclinical and clinical evidence that substantiates the effectiveness of NF-κB inhibitors in treating AMD by diminishing inflammation and pathological angiogenesis. •NF-κB drives inflammation and angiogenesis in age-related macular degeneration (AMD).•NF-κB activation in AMD induces pro-inflammatory cytokines and immune cell transfer.•NF-κB stimulates VEGF production, promoting neovascular vessel formation in AMD.•Targeting NF-κB could be therapeutic, reducing inflammation and angiogenesis in AMD.•Preclinical and clinical data support NF-κB inhibitors for managing AMD effectively.