Abstract
Proliferative vitreoretinopathy (PVR) is thought to represent an exaggerated and protracted scarring process following rhegmatogenous retinal detachment (RD) and following RD surgery. Following detachment, a combination of retinal ischaemia, inflammation and cell proliferation lead to the formation of tractional membranes on the epiretinal and subretinal surfaces and to marked gliosis within the retina that leads to retinal shortening. Both of these factors convert a rhegmatogenous RD into a tractional one are a major feature of RD surgery failure. The major cell types that are involved in PVR are retinal pigment epithelium (RPE), glial cells (principally Muller cells) and inflammatory cells (macrophages and lymphocytes). These cells interact with numerous growth factors and cytokines derived from the breakdown of the blood–retinal barrier and from vitreous contact that trigger a cascade of cellular processes, such as epithelial–mesenchymal transition (EMT), cell migration, chemotaxis, proliferation, elaboration of basement membrane and collagen and cellular contraction, that lead to overt retinal pathology. This review covers the histopathology of PVR and touches upon the cellular processes involved in the pathogenesis of PVR.
摘要
增殖性玻璃体视网膜病变 (PVR) 为孔源性视网膜脱离 (RD) 和RD手术后的过度而持久的瘢痕形成过程。视网膜脱离后, 由视网膜缺血、炎症和细胞增殖共同导致了视网膜表面和视网膜下形成了牵拉性增殖膜, 造成视网膜纤维增生并导致视网膜皱缩 。这些因素将孔源性RD转变为牵拉性RD, 是RD手术失败的主要特征。在PVR的病理形成中主要包括视网膜色素上皮 (RPE) 细胞、胶质细胞 (主要为Muller细胞) 和炎性细胞 (巨噬细胞和淋巴细胞) 。这些细胞与其它来源于血视网膜屏障破坏和玻璃体的大量生长因子和细胞因子相互作用, 触发细胞级联反应, 如上皮-间质转化 (EMT) 、细胞迁移、趋化、增殖, 基底膜与胶原的修饰以及细胞的收缩从而导致视网膜病变。本文综述了PVR的组织病理学以及各种细胞在PVR病理发病机制中的作用。
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Mudhar, H.S. A brief review of the histopathology of proliferative vitreoretinopathy (PVR). Eye 34, 246–250 (2020). https://doi.org/10.1038/s41433-019-0724-4
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DOI: https://doi.org/10.1038/s41433-019-0724-4
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