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特发性视网膜前膜形成的炎症机制。

Inflammatory mechanisms of idiopathic epiretinal membrane formation.

机构信息

Department of Ophthalmology, University of Arizona Medical Center, Tucson, AZ 85711, USA.

出版信息

Mediators Inflamm. 2013;2013:192582. doi: 10.1155/2013/192582. Epub 2013 Nov 11.

Abstract

The pathogenesis of idiopathic epiretinal membranes (iERMs), a common pathology found in retina clinics, still eludes researchers to date. Ultrastructural studies of iERMs in the past have failed to identify the cells of origin due to the striking morphologic changes of cells involved via transdifferentiation. Thus, immunohistochemical techniques that stain for the cytostructural components of cells have confirmed the importance of glial cells and hyalocytes in iERM formation. The cellular constituents of iERMs are thought to consist of glial cells, fibroblasts, hyalocytes, etc. that, in concert with cytokines and growth factors present in the vitreous, lead to iERM formation. Recently, research has focused on the role of the posterior hyaloid in iERM formation and contraction, particularly the process of anomalous PVD as it relates to iERM formation. Recent advances in proteomics techniques have also elucidated the growth factors and cytokines involved in iERM formation, most notably nerve growth factor, glial cell line-derived growth factor, and transforming growth factor β1.

摘要

特发性视网膜内细胞层膜(iERM)的发病机制仍然是目前研究的难点,这是一种在视网膜诊所常见的病症。过去对 iERM 的超微结构研究由于涉及细胞的显著形态变化而未能确定细胞的起源,这些变化是通过转分化引起的。因此,免疫组织化学技术对细胞的细胞结构成分进行染色,证实了胶质细胞和玻璃体细胞在 iERM 形成中的重要性。iERM 的细胞成分被认为包括胶质细胞、成纤维细胞、玻璃体细胞等,这些细胞与玻璃体内存在的细胞因子和生长因子一起,导致 iERM 的形成。最近的研究集中在后部玻璃体液在 iERM 形成和收缩中的作用上,特别是与 iERM 形成相关的异常 PVD 过程。蛋白质组学技术的最新进展也阐明了参与 iERM 形成的生长因子和细胞因子,其中最显著的是神经生长因子、胶质细胞系衍生的生长因子和转化生长因子β1。

相似文献

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Inflammatory mechanisms of idiopathic epiretinal membrane formation.特发性视网膜前膜形成的炎症机制。
Mediators Inflamm. 2013;2013:192582. doi: 10.1155/2013/192582. Epub 2013 Nov 11.
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Cellular components of the idiopathic epiretinal membrane.特发性视网膜前膜的细胞成分
Graefes Arch Clin Exp Ophthalmol. 2022 May;260(5):1435-1444. doi: 10.1007/s00417-021-05492-7. Epub 2021 Nov 29.

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