Abstract:

According to the latest study, the initial mechanisms implicated in proliferative vitreoretinopathy (PVR) is part of the nonspecific tissue repair process of retinal reconstruction. After retinal separation, the retinal outer layers become ischemic and the photoreceptors start to die by several pathways, but mainly apoptosis. This loss of neurons stimulates the hypertrophy of retinal glial cells (mainly Müller cells), but also astrocytes and microglia, that begin the remodeling of the retina and perhaps the neuroprotection of the remaining neurons. However， these intraretinal changes cause the substitution of neurons by glial tissue and  shortening of the retina. As part of tissue remodeling, the process of PVR is triggered by glial cells. Frequently, RPE cells de-differentiate into fibroblast- or macrophage-like cell morphology. In this process, contractile cellular or fibrocellular membranes are created, preventing retinal reattachment. We propose to identify and name this process as intraretinal PVR.(Int Rev Ophthalmol,  2017,  41:    92-95)