Vascular Endothelial Growth Factor Signaling in Fibrosis: An Ophthalmic Perspective |Biomedgrid

Fibrosis is a common condition, transcending all areas of medicine. Its pathophysiology has eluded researchers for decades with no universal cure. The cellular processes which underpin these conditions begin with cellular proliferation, followed by migration, epithelial to mesenchymal transformation, and extracellular matrix contraction. This short review highlights the complexities in the signaling cascade of the key event in fibrosis: epithelial to mesenchymal transition with particular emphasis on the role of vascular endothelial growth factor (VEGF). Other growth factors, mitogens, and markers of fibrosis included in this review are transforming growth factor β (beta), platelet-derived growth factor, cadherins, Smads, Slug, Snail, α-SMA, and the Rho-kinase group, among others. The ocular lens capsule serves as an ideal model to study this pathophysiology due to its isolation from other organs, avascular environment, and experimental models available. Anti-VEGF treatments are well established for neovascular conditions such as age-related macular degeneration and may therefore form a component of anti-fibrotic treatment in the future. Evidence for reduction of fibrotic markers following VEGF inhibition is revealed last.