Pharmacological strategies for the prevention and treatment of proliferative vitreoretinopathy: A comprehensive review.

Abstract

Proliferative vitreoretinopathy (PVR) represents the most significant complication and the primary cause of surgical failure in regmatogenous retinal detachment repair, occurring in approximately 5-10% of cases. The pathophysiology of PVR involves a counterproductive wound-healing response where retinal pigment epithelium and glial cells undergo dedifferentiation, migration, and proliferation. This process is largely driven by epithelial-to-mesenchymal transition (EMT) and a complex milieu of inflammatory mediators and growth factors, most notably platelet-derived growth factor and transforming growth factor beta. We investigate the evolving role of adjuvant pharmacotherapy in preventing and treating PVR. Traditional anti-inflammatory agents and anti-vascular endothelial gowth facrtor therapies have failed to demonstrate significant improvements in anatomical reattachment rates in human clinical trials. Conversely, anti-proliferative agents have shown more clinical potential; specifically, methotrexate has emerged as a leading candidate. Other promising strategies include the use of combined 5-fluorouracil and low molecular weight heparin, daunorubicin, and emerging biological therapies such as Rho Kinase and m-TOR inhibitors. Furthermore, innovative bio-functional polymers are being developed to modulate RNA transcription and suppress EMT factors. Therefore, PVR management is shifting toward a multimodal paradigm that integrates advanced surgical techniques with targeted molecular inhibition to improve functional success.