Jakobs Tatjana C
Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts 02114.
Cold Spring Harb Perspect Med. 2014 Jul 1;4(7):a020636. doi: 10.1101/cshperspect.a020636.
In glaucoma, regardless of its etiology, retinal ganglion cells degenerate and eventually die. Although age and elevated intraocular pressure (IOP) are the main risk factors, there are still many mysteries in the pathogenesis of glaucoma. The advent of genome-wide microarray expression screening together with the availability of animal models of the disease has allowed analysis of differential gene expression in all parts of the eye in glaucoma. This review will outline the findings of recent genome-wide expression studies and discuss their commonalities and differences. A common finding was the differential regulation of genes involved in inflammation and immunity, including the complement system and the cytokines transforming growth factor β (TGFβ) and tumor necrosis factor α (TNFα). Other genes of interest have roles in the extracellular matrix, cell-matrix interactions and adhesion, the cell cycle, and the endothelin system.
在青光眼患者中，无论其病因如何，视网膜神经节细胞都会发生退化并最终死亡。尽管年龄和眼压升高是主要危险因素，但青光眼的发病机制仍存在许多谜团。全基因组微阵列表达筛选技术的出现以及该疾病动物模型的可得性，使得人们能够分析青光眼患者眼部各部位的差异基因表达。本综述将概述近期全基因组表达研究的结果，并讨论它们的共性与差异。一个共同的发现是，参与炎症和免疫的基因存在差异调节，包括补体系统以及细胞因子转化生长因子β（TGFβ）和肿瘤坏死因子α（TNFα）。其他受关注的基因在细胞外基质、细胞 - 基质相互作用与黏附、细胞周期以及内皮素系统中发挥作用。
