Age-Related Macular Degeneration: A Disease of Cellular Senescence and Dysregulated Immune Homeostasis.

Age-related macular degeneration (AMD) is a degenerative ocular disease primarily affecting central vision in the elderly. Its pathogenesis is complex, involving cellular senescence and immune homeostasis dysregulation. This review investigates the interaction between these two critical biological processes in AMD pathogenesis and their impact on disease progression. Initially, cellular senescence is analyzed, with particular emphasis on retinal damage induced by senescent retinal pigment epithelial cells. Subsequently, the occurrence of immune homeostasis dysregulation within the retina and its mechanistic role in AMD areis explored. Furthermore, the paper also discusses in detail the interplay between cellular senescence and immune responses, forming a vicious cycle that exacerbates retinal damage and may influence treatment outcomes. In summary, a deeper understanding of the interrelation between cellular senescence and immune dysregulation is vital for the developing innovative therapeutic strategies for AMD.

Research progress of iron metabolism in retinal diseases.

Background: Retinal diseases can lead to severe visual impairment and even blindness, but current treatments are limited. For precise targeted therapy, the pathophysiological mechanisms of the diseases still need to be further explored. Iron serves an essential role in many biological activities and helps maintain the function and morphology of the retina. The vision problems caused by retinal diseases are affecting more and more people, the study of iron metabolism in retinal diseases possesses great potential for clinical application. Main text: Iron maintains a dynamic balance in the retina but in excess is toxic to the retina. Iron overload can lead to various pathological changes in the retina through oxidative stress, inflammation, cell death, angiogenesis and other pathways. It is therefore involved in the progression of retinal diseases such as age-related macular degeneration, glaucoma, diabetic retinopathy, retinitis pigmentosa, and hereditary iron overload. In recent years, iron chelators have been shown to be effective in the treatment of retinal diseases, but the exact mechanism is not yet fully understood. This question prompted further investigation into the specific mechanisms by which iron metabolism is involved in retinal disease. Conclusions: This review summarizes iron metabolism processes in the retina and mechanistic studies of iron metabolism in the progression of retinal disease. It also highlights the therapeutic potential of iron chelators in retinal diseases.