Abstract: Age-related macular degeneration (AMD) is a leading cause of global blindness and currently remains incurable. Accumulating evidence suggests that alterations in lipid homeostasis may contribute to the pathogenesis of AMD. Lipid metabolism supplies energy to the retina, contributes to cellular structure, and maintains cellular homeostasis. Specifically, imbalances in circulating lipoproteins have been implicated in the onset of AMD. Lipid metabolism influences AMD progression through mechanisms such as lipofuscin accumulation, mitochondrial dysfunction, and neovascularization.Among lipid metabolism genes,the protective allele of the ATP-binding cassette transporter A1 can enhance cholesterol excretion and reduce lipid deposition, while the risk variant weakens this function. The ε4 allele of apolipoprotein E is an important protective factor for AMD and may be related to the promotion of lipid clearance. The ε2 allele is usually associated with an increased risk. There are also opposite-effect loci for the cholesterol ester transfer protein and liver lipase C genes. By understanding the role of lipids in the development and maintenance of AMD, developing treatment methods targeting lipid metabolism-related AMD can provide new solutions for the treatment of AMD related to lipid metabolism.

Key words: Age-related macular degeneration, Lipid metabolism, Retina