Cellular senescence in the glaucomatous outflow pathway
Cellular senescence in the glaucomatous outflow pathway
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DOI：
10.1016/j.exger.2005.06.005
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发表时间：
2005-08-01
影响因子：
3.9
通讯作者：
Gonzalez, P
中科院分区：
文献类型：
--
作者：
Liton, PB;Challa, P;Gonzalez, P
原发性开角型青光眼（POAG）中小梁网（TM）-施累姆氏管（SC）传统流出道组织进行性功能障碍的机制仍不完全清楚。为了确定POAG是否以衰老细胞的积累为特征，类似于在其他疾病中所描述的，我们比较了POAG和年龄匹配的对照供体的流出通路细胞中衰老标记物衰老相关β-半乳糖苷酶（SA-β-gal）的水平。POAG供体显示SA-β-gal阳性细胞百分比的统计学显著性增加四倍。这些结果表明细胞衰老在流出途径的病理生理学中的潜在作用。(c)2005年爱思唯尔公司All rights reserved.
The mechanisms responsible for the progressive malfunction of the trabecular meshwork (TM)-Schlemm's canal (SC) conventional outflow pathway tissue in primary open angle glaucoma (POAG) are still not fully understood. To determine whether POAG is characterized by an accumulation of senescent cells, similar to what has been described in other diseases, we have compared the levels of the senescence marker senescence-associated-beta-galactosidase (SA-beta-gal) in the outflow pathway cells of POAG and age-matched control donors. POAG donors demonstrated a statistically significant fourfold increase in the percentage of SA-beta-gal positive cells. These results suggest a potential role for cellular senescence in the pathophysiology of the outflow pathway. (c) 2005 Elsevier Inc. All rights reserved.