Abstract
Myopia has become a global public health challenge, with pathological high myopia leading to irreversible visual impairment. Accumulating evidence suggests that chronic inflammation is closely associated with scleral remodeling and axial elongation, the primary pathological features of myopia progression. This mini review systematically summarizes the epidemiological associations between local (ocular tissue-specific) and systemic inflammatory responses with myopia, highlighting key inflammatory mediators (NF-κB, MMP-2, IL-6, TNF-α) and their synergistic mechanisms in modulating scleral extracellular matrix degradation. We further dissect the molecular cascade of "mechanical stress - inflammation activation - ECM remodeling - fibroblast-myofibroblast transformation" that underpins myopic scleral weakening. Current research limitations include inadequate translation of animal model findings to humans, a lack of non-invasive inflammatory monitoring tools, and unstandardized biomarkers. Future directions should leverage multi-omics technologies to decode complex inflammatory networks and the gut-retina axis, facilitating the development of stage-specific precision anti-inflammatory interventions. This review offers novel insights into the inflammatory mechanisms underlying myopia and provides a theoretical basis for clinical prevention and treatment strategies.