Wiedemann P, Weller M, Heimann K
Klinik und Poliklinik für Augenheilkunde, Universität zu Köln.
Klin Monbl Augenheilkd. 1990 Nov;197(5):355-61. doi: 10.1055/s-2008-1046292.
In this article the authors review present knowledge concerning the pathogenesis of proliferative vitreoretinopathy (PVR). The function of cells such as macrophages, fibroblasts, retinal pigment epithelial cells, and glial cells, as well as their interaction with constituents of the extracellular matrix such as fibronectin, vitronectin, and factor XIII, are described. Current data on growth factor involvement in the pathogenesis of PVR are explained. Attention is focused on the histopathological differences between traumatic and idiopathic membranes, "young" and "old" membranes, and PVR and diabetic membranes. On the basis of the findings presented, the importance of the breakdown of the blood-retinal barrier, the participation of the coagulation system, and immunological aspects of membrane formation are discussed. Conceivable new strategies for medical treatment of PVR are proposed.
在本文中,作者回顾了关于增殖性玻璃体视网膜病变(PVR)发病机制的现有知识。描述了巨噬细胞、成纤维细胞、视网膜色素上皮细胞和神经胶质细胞等细胞的功能,以及它们与细胞外基质成分如纤连蛋白、玻连蛋白和因子XIII的相互作用。解释了关于生长因子参与PVR发病机制的当前数据。重点关注创伤性和特发性膜、“年轻”和“老”膜以及PVR和糖尿病性膜之间的组织病理学差异。根据所呈现的研究结果,讨论了血视网膜屏障破坏、凝血系统参与以及膜形成的免疫学方面的重要性。提出了PVR药物治疗可能的新策略。