Abstract
Background: Pterygium is characterized by the overgrowth of fibroblasts and the remodeling of the extracellular matrix (ECM), driven by MMPs. The review outlines the pathophysiology of pterygium, emphasizing the role of MMP-3 in cell motility, proteolysis, and angiogenesis. The recurrence rate of pterygium following surgical excision remains a significant challenge, with current adjuvant therapies like mitomycin-C presenting serious side effects. Methods: The review synthesizes findings from various studies on the effects of EGCG on MMP-3 expression and fibroblast migration. It discusses the mechanisms by which EGCG inhibits MMP-3 activity and its potential impact on pterygium progression. Findings: EGCG has been shown to inhibit MMP-3 expression and activity in several models, including mouse Lewis lung carcinoma-derived cells and photoaged hairless mouse models. It also suppresses the migration of human pterygium fibroblast cells, potentially preventing pterygium formation. EGCG's ability to reduce oxidative stress and modulate inflammatory pathways further supports its therapeutic potential. Conclusion: EGCG emerges as a promising agent for inhibiting MMP-3 expression and human pterygium fibroblast migration, offering a safer alternative to current adjuvant therapies. Its anti-inflammatory, antioxidant, and anti-angiogenic properties make it a potential therapeutic option for managing pterygium, warranting further clinical investigation.
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