Welge-Lüssen U, Birke K
Augenklinik, Universität Erlangen-Nürnberg.
Klin Monbl Augenheilkd. 2010 Feb;227(2):99-107. doi: 10.1055/s-0029-1245171. Epub 2010 Feb 12.
Primary open angle glaucoma (POAG) is defined as an optic neuropathy which is characterised by the loss of optic nerve axons and the related retinal ganglion cells. The reason for these changes is still unknown. In the pathogenesis of POAG several factors like increased intraocular pressure and a reduction of ocular blood supply are discussed. Morphological and biochemical analyses of the trabecular meshwork (TM) of POAG patients revealed loss of cells, increased accumulation of extracellular matrix (ECM), changes in the cytoskeleton, cellular senescence and the process of subclinical inflammation. One factor becoming more likely to be involved in the pathogenesis of POAG is oxidative stress. Treatment of TM cells with oxidative stress induced POAG-typical changes like ECM accumulation, cell death, disarrangement of the cytoskeleton, advanced senescence and the release of inflammatory markers. By pretreatment with antioxidants, prostaglandin analogues, beta-blockers or local carbonic anhydrase inhibitors, these effects were markedly reduced. In conclusion, oxidative stress is able to induce characteristic glaucomatous TM changes in vitro and these oxidative stress-induced TM changes can be minimised by the use of antioxidants and IOP-lowering substances. It is tempting to speculate that prevention of oxidative stress exposure to the TM may help to reduce the progression of POAG.
原发性开角型青光眼（POAG）被定义为一种视神经病变，其特征是视神经轴突及相关视网膜神经节细胞的丧失。这些变化的原因尚不清楚。在POAG的发病机制中，讨论了诸如眼内压升高和眼部血液供应减少等几个因素。对POAG患者小梁网（TM）的形态学和生化分析显示细胞丢失、细胞外基质（ECM）积累增加、细胞骨架变化、细胞衰老以及亚临床炎症过程。氧化应激越来越有可能参与POAG的发病机制。用氧化应激处理TM细胞会诱导出POAG典型的变化，如ECM积累、细胞死亡、细胞骨架紊乱、衰老加剧以及炎症标志物的释放。通过用抗氧化剂、前列腺素类似物、β受体阻滞剂或局部碳酸酐酶抑制剂进行预处理，这些影响会明显降低。总之，氧化应激能够在体外诱导典型的青光眼性TM变化，并且通过使用抗氧化剂和降低眼压的物质可以将这些氧化应激诱导的TM变化降至最低。人们不禁推测，防止TM暴露于氧化应激可能有助于减少POAG的进展。
