早期视网膜内增生性玻璃体视网膜病变的发病机制

vitreoretinopathy The pathogenesis of early intraretinal proliferative

增生性玻璃体视网膜病变（proliferative vitreoretinopathy，PVR）是视网膜重建的非特异性组织修复过程中的一部分。它发生在视网膜脱离后，视网膜外层缺血，光感受器细胞逐渐死亡（主要是凋亡），神经元丢失并刺激胶质细胞（主要是Muller细胞）肥大，视网膜也开始重建及保护余下的神经元，但这一系列反应如果过度，胶质组织就会代替神经元，视网膜也会受到牵拉而缩短，发生早期的PVR改变。整个过程中，胶质细胞起始了PVR，之后视网膜色素上皮细胞发生去分化，转化为巨噬细胞或成纤维细胞样形态，之后细胞或纤维膜发生收缩，阻止了视网膜的复位，PVR随之发生。这个过程我们称之为早期视网膜内增生性玻璃体视网膜病变。

According to the latest study, the initial mechanisms implicated in proliferative vitreoretinopathy （PVR） is part of the nonspeeific 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 Mtiller 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 fibrnblastor 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.