Huang Wenbin, Fan Qian, Wang Wei, Zhou Minwen, Laties Alan M, Zhang Xiulan
Zhongshan Ophthalmic Center, State Key Laboratory of Ophthalmology, Sun Yat-sen University, PR China.
Med Sci Monit Basic Res. 2013 Sep 4;19:237-40. doi: 10.12659/MSMBR.889061.
Numerous studies have been completed on glaucoma pathogenesis. However, the potential and controversial interaction between ocular biomechanical properties and the glaucomatous diseases process has received much more attention recently. Previous studies have found that collagen tissues gain mutation change in glaucoma patients. This study was conducted to determine the role of collagen in the biomechanics of glaucoma in humans. Its changes may be the result of mechanical modifications brought on by intraocular pressure (IOP) fluctuations. More importantly, biomechanics and genetic evidence indicate that the mutation of collagen may play a role in the process of glaucoma. Alteration of collagen in the outflow pathway may alter mechanical tissue characteristics and a concomitant increase of aqueous humor outflow resistance and elevation of IOP. The variations of collagen, leading to inter-individual differences in scleral and lamina cribrosa properties, result in different susceptibility of individuals to elevated IOP. Therefore, this study hypothesized that collagen mutations may be an original cause of glaucoma.
关于青光眼发病机制已完成了大量研究。然而，眼生物力学特性与青光眼疾病进程之间潜在且存在争议的相互作用近来受到了更多关注。先前的研究发现青光眼患者的胶原组织存在突变变化。本研究旨在确定胶原在人类青光眼生物力学中的作用。其变化可能是眼内压（IOP）波动引起的机械改变的结果。更重要的是，生物力学和遗传学证据表明胶原突变可能在青光眼进程中起作用。房水流出途径中胶原的改变可能会改变组织的机械特性，并伴随房水流出阻力增加和眼压升高。胶原的变化导致巩膜和筛板特性的个体差异，导致个体对眼压升高的易感性不同。因此，本研究假设胶原突变可能是青光眼的一个原发性病因。
