Abstract
Myopia is an evolving global health challenge, with estimates suggesting that by 2050 it will affect half of the world's population, becoming the leading cause of irreversible vision loss. Moreover, myopia can lead to various complications, including the earlier onset of cataracts. Given the progressive aging of the population and the increase in life expectancy, this will contribute to a rising demand for cataract surgery, posing an additional challenge for healthcare systems. The pathogenesis of nuclear and posterior subcapsular cataract (PSC) development in axial myopia is complex and primarily involves intensified liquefaction of the vitreous body, excessive production of reactive oxygen species, impaired antioxidant defense, and chronic inflammation in the eyeball. These factors contribute to disruptions in mitochondrial homeostasis, abnormal cell signaling, lipid peroxidation, protein and nucleic acid damage, as well as the induction of adverse epigenetic modifications. Age-related and oxidative processes can cause destabilization of crystallins with subsequent protein accumulation, which finally drives to a lens opacification. Moreover, an altered redox status is one of the major contributors to the pathogenesis of PSC. This review aims to summarize the mechanisms known to be responsible for the accelerated development of cataracts in axial myopia and to enhance understanding of these relationships.