Liton Paloma B, Lin Yizhi, Gonzalez Pedro, Epstein David L
Department of Ophthalmology, Duke University, Durham, NC 27710, USA.
Autophagy. 2009 Jan;5(1):122-4. doi: 10.4161/auto.5.1.7304. Epub 2009 Jan 31.
Primary open angle glaucoma (POAG) is a late onset disease usually accompanied by elevated intraocular pressure (IOP) that results from the failure of the trabecular meshwork (TM) to maintain normal levels of aqueous humor outflow resistance. Cells in the TM are subjected to chronic oxidative stress through reactive oxygen species (ROS) present in the aqueous humor (AH) and generated by normal metabolism. Exposure to ROS is thought to contribute to the morphological and physiological alterations of the outflow pathway in aging and POAG. Our results indicate that chronic exposure of TM cells to oxidative stress causes the accumulation of nondegradable material within the lysosomal compartment leading to diminished lysosomal activity and increased SA-beta-Gal expression. Because the lysosomal compartment is responsible for maintaining general cellular turnover, such impaired activity may lead to a progressive cellular decline in the TM cell function and thus contribute to the progression of POAG.
原发性开角型青光眼（POAG）是一种迟发性疾病，通常伴有眼压（IOP）升高，这是由于小梁网（TM）无法维持正常水平的房水流出阻力所致。TM中的细胞通过房水（AH）中存在的活性氧（ROS）以及正常代谢产生的ROS遭受慢性氧化应激。暴露于ROS被认为会导致衰老和POAG中流出途径的形态和生理改变。我们的结果表明，TM细胞长期暴露于氧化应激会导致溶酶体隔室内不可降解物质的积累，从而导致溶酶体活性降低和SA-β-Gal表达增加。由于溶酶体隔室负责维持细胞的一般更新，这种受损的活性可能导致TM细胞功能逐渐衰退，从而促进POAG的进展。
