Relationship between choroidal thickness changes and macrophage polarization in high myopia

High myopia is one of the major causes of blindness worldwide, and the pathological mechanism underlying its characteristic progressive choroidal thinning has long been a research focus. Traditional views have mostly attributed choroidal thinning to the passive result of mechanical stretch caused by axial elongation or insufficient choroidal blood perfusion. With deeper research, increasing evidence suggests that an active and dynamic immune-inflammatory remodeling process may exist in the choroid. By systematically reviewing recent findings in myopia and immunology, and integrating evidence from clinical imaging, intraocular fluid analyses, and animal experiments, this review attempts to construct a pathological framework centered on the following core sequence: "mechanical stretch/relative hypoxic stress-immune microenvironment imbalance-macrophage polarization-destructive choroidal remodeling." This article focuses on how macrophages may become polarized after sensing mechanical stretch and hypoxic signals, and how these changes may contribute to choroidal structural and functional degeneration through cytokine secretion, regulation of matrix metabolism, and mediation of vascular regression. In addition, this review summarizes areas that still need improvement, including human tissue data and evidence from macrophage subset-specific interventions, and discusses future directions such as spatial transcriptomics and targeted immune modulation, with the aim of deepening the understanding of the pathological mechanisms of high myopia and providing references for the development of new prevention and treatment strategies.