Purpose of review: Despite advancement in the surgical instrumentation and techniques, proliferative vitreoretinopathy (PVR) remains the most common cause for failure of rhegmatogenous retinal detachment (RRD) repair. This review discusses ongoing translational and clinical advancements in PVR.
Recent findings: PVR represents an exaggerated and protracted scarring process that can occur after RRD. The primary cell types involved are retinal pigment epithelium, glial, and inflammatory cells. They interact with growth factors and cytokines derived from the breakdown of the blood-retinal barrier that trigger a cascade of cellular processes, such as epithelial-mesenchymal transition, cell migration, chemotaxis, proliferation, elaboration of basement membrane and collagen and cellular contraction, leading to overt retinal pathology. Although there are currently no medical therapies proven to be effective against PVR in humans, increased understanding of the risks factors and pathophysiology have helped guide investigations for molecular targets of PVR. The leading therapeutic candidates are drugs that mitigate growth factors, inflammation, and proliferation are the leading therapeutic candidates.
Summary: Although multiple molecular targets have been investigated to prevent and treat PVR, none have yet demonstrated substantial evidence of clinical benefit in humans though some show promise. Advancements in our understanding of the pathophysiology of PVR may help develop a multipronged approach for this condition.
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