Inhibition of the Post-Trabeculectomy Wound Healing Process by Epigallocatechin-3-Gallate (EGCG) through Regulation of Matrix Metalloproteinase-3 (MMP-3) Expression and Fibroblast Migration in Human Tenon Fibroblasts

Abstract

This review investigates the role of Epigallocatechin-3-gallate (EGCG) in inhibiting wound healing through the regulation of matrix metalloproteinase-3 (MMP-3) expression and fibroblast migration in human Tenon fibroblasts. Glaucoma, a chronic optic neuropathy characterized by optic nerve degeneration, often necessitates surgical interventions such as glaucoma filtration surgery (GFS) due to persistent vision loss despite initial treatments aimed at reducing intraocular pressure (IOP). However, excessive wound healing and fibrosis significantly contribute to a surgical failure rate of 35-43%. This review highlights that excessive fibrosis in the subconjunctival bleb region is a primary cause of post-trabeculectomy failure, with failure rates ranging from 24% to 74% within four years post-surgery. The findings suggest that EGCG may play a crucial role in modulating the wound healing process by influencing the behavior of Tenon fibroblast cells, which are essential for wound healing and fibrotic tissue formation. By regulating MMP-3 expression and fibroblast migration, EGCG presents a potential therapeutic avenue to mitigate fibrosis and improve surgical outcomes in glaucoma treatment. In conclusion, this review underscores the importance of understanding the mechanisms by which EGCG affects wound healing, potentially leading to more effective strategies for managing fibrosis in glaucoma surgeries