Endothelial cell senescence contributes to pathological retinal angiogenesis

BackgroundPathological retinal neovascularization is marked by microvascular lesions manifested initially as endothelial cell dysfunction and metabolic disturbances. However, the regulatory mechanism guiding retinal vascular endothelial cell function remian controversial.Main bodyPrevious studies have demonstarted that high glucose or oxidative stress can induce premature senescence in endothelial cells, triggering inflammatory responses within the vascular system and promoting the secretion of pro-inflammatory factors, ultimately leading to pathological angiogenesis. Endothelial cell senescence has thus become a key target for anti-angiogenic therapies.ConclusionThis review delves into current research on the mechanisms driving senescence-induced retinal angiogenesis and highlights potential target protein pathways, aiming to provide insights for future investigations. High glucose or oxidative stress promotes reactive oxygen species accumulation in retinal endothelial cells and induces cell senescence.The senescent endothelial cells exhibited the secretion phenotype of senescence-related secretory phenotype and increased senescence-associated proteins.Targeting forkhead family 'O' group/Sirtuins and cGAS/STING signalling pathways to inhibit endothelial cell senescence may be a new therapy for anti-angiogenesis. image