Abstract:

The pathogenesis of proliferative vitreoretinopathy (PVR) is not totally clear. Vascular endothelial growth factor (VEGF) was demonstrated to be increased in vitreous and epiretinal membranes of patients with PVR and animal PVR models. In animal PVR models, anti-VEGF therapy could effectively prevent the development of PVR. The mechanism of VEGF promoting the development of PVR may be that VEGF competes with platelet-derived growth factor (PDGF) for binding to platelet-derived growth factor receptor α (PDGFR-α). VEGF therefore increases the pool of monomeric PDGFR-α available to be indirectly activated by growth factors outside PDGF (non-PDGFs), stimulating signaling pathways such as PI3K/Akt, which reduces the level of p53.