Age-related macular degeneration (AMD) is a leading cause of blindness among the elderly, characterized by the degeneration of retinal pigment epithelial cells and the death of photoreceptors. The pathogenesis of AMD is complex, involving a multitude of factors, including genetic, environmental, and metabolic influences. Cellular senescence serves as a significant risk factor for AMD, where cells enter a permanent state of cell cycle arrest after a limited number of divisions. As age increases, the accumulation of senescent cells is closely associated with various age-related chronic diseases. Key mechanisms underlying cellular senescence include oxidative stress, DNA damage, mitochondrial dysfunction, defects in autophagy and mitophagy, and epigenetic alterations. In the context of AMD, various cell types-including pigment epithelial cells, vascular endothelial cells, cells of Bruch's membrane, photoreceptors, and microglia-exhibit signs of senescence and related changes. Cellular senescence plays a pivotal role in the pathogenesis of AMD, contributing to the degeneration of different retinal cell types and supporting vascular systems. By thoroughly investigating these mechanisms, there is hope for the development of more effective therapies aimed at restoring and protecting vision in affected patients. This article reviews the biological mechanisms of cellular senescence and its role in AMD, exploring how different cell types contribute to the disease's onset, with the goal of providing new insights into the pathogenesis and treatment of AMD.
