Abstract: The characteristic change of age-related macular degeneration (AMD) is the lipid deposits and drusen in Bruch’s membrane. Therefore, the formation of AMD lesions is considered to be related to lipid metabolism. The decrease of dietary omega-3 long-chain polyunsaturated fatty acids (omega-3 LC-PUFAs) intake and the increase of the circulating high-density lipoprotein cholesterol are associated with the increased risk of AMD. Some gene variations of lipid metabolism are associated with the risk of AMD, but not all the gene variants that increase the concentration of circulating high-density lipoprotein will increase the risk of AMD. Retinal lipids maintain its homeostasis through uptake from circulatory system, autophagy degradation, local synthesis，secretion and outflow. When the retinal lipids homeostasis changes, local lipid accumulation and peroxidation takes place, and finally the characteristic inflammatory lesions of AMD appears. However, the role of lipid granules and whether local or circulating HDL-C or both are involved in the pathogenesis of AMD are not clear. In addition, the results of omega-3 LC PUFAs and lipid-regulatory drugs in the treatment of AMD are inconsistent, which need further study. (Int Rev Ophthalmol, 2021, 45: 346-350)

Key words: age-related macular degeneration, high-density lipoprotein cholesterol, dietary lipids, circulating lipoproteins, retinal lipids, genetics