The global prevalence of myopia is becoming increasingly severe, with epidemiological models predicting that by 2050, approximately 50% of the world’s population will be affected by myopia, and about 10% will suffer from high myopia. The incidence of high myopia is projected to increase fivefold, making it the leading cause of irreversible vision impairment. Myopia often leads to various complications and has been associated with other ocular diseases, including early-onset cataracts, age-related macular degeneration, and primary open angle glaucoma. As a result, the control and management of myopia have become ongoing and long-term research priorities. The pathogenesis of myopia involves complex multisystem interactions. Current mainstream theories focus primarily on choroidal hypoxia-induced scleral remodeling, with neurotransmitters such as acetylcholine and dopamine playing regulatory roles. However, recent studies have increasingly suggested that changes in nutritional intake, including proteins, fats, and cholesterol, may also be related to myopia development. The role of lipid metabolism in the onset and progression of myopia has gradually attracted growing attention. Therefore, this review aims to systematically elucidate the molecular mechanisms of lipid metabolism regulatory networks in axial myopia, integrating multidimensional factors to provide a theoretical foundation for precision intervention strategies.