Gabelt B'Ann True, Kaufman Paul L
Department of Ophthalmology and Visual Sciences, University of Wisconsin, F4/340 CSC, 600 Highland Avenue, Madison, WI 53792-3220, USA.
Prog Retin Eye Res. 2005 Sep;24(5):612-37. doi: 10.1016/j.preteyeres.2004.10.003.
Changes in aqueous humor dynamics with age and in glaucoma have been studied for several decades. More recently, techniques have been developed which confirm earlier studies showing that outflow facility decreases with age and in glaucoma and add the newer finding that uveoscleral outflow also decreases. Morphologic studies in aging and glaucoma eyes have shown an increase in accumulation of extracellular material in both the trabecular meshwork and ciliary muscle and a loss of trabecular meshwork cells, which contribute to this reduction in outflow and result in an increase in intraocular pressure. A reduction in hyaluronic acid and increases in fibronectin and thrombospondin contribute to the change in the extracellular environment. Imbalances in responses to age-related stresses such as oxidative damage to long-lived molecules, protein cross-linking and loss of elasticity could trigger excess production of factors such as transforming growth factor beta, interleukin-1 and CD44S that could stimulate pathways leading to increases in fibronectin, transformation of trabecular meshwork cells to a myoepithelial state and decrease the breakdown in extracellular matrix material, allowing excess to accumulate. Ultimately trabecular outflow and uveoscleral outflow are reduced and intraocular pressure becomes elevated, adding more stress and perpetuating the pathological condition. Future research to identify additional factors and clarify their roles in these processes could lead to alternative therapies for age and glaucoma related changes in the eye.
几十年来，人们一直在研究房水动力学随年龄增长及青光眼的变化情况。最近，已开发出一些技术，这些技术证实了早期的研究结果，即随着年龄增长及患青光眼，房水流出易度会降低，并且还发现了新的现象，即葡萄膜巩膜途径的房水流出也会减少。对衰老和青光眼患者眼睛的形态学研究表明，小梁网和睫状肌中细胞外物质的积累增加，小梁网细胞丢失，这导致房水流出减少，进而导致眼压升高。透明质酸减少，纤连蛋白和血小板反应蛋白增加，导致细胞外环境发生变化。对与年龄相关应激的反应失衡，如对长寿分子的氧化损伤、蛋白质交联和弹性丧失，可能会引发诸如转化生长因子β、白细胞介素 -1 和 CD44S 等因子的过量产生，这些因子会刺激导致纤连蛋白增加、小梁网细胞转化为肌上皮状态的途径，并减少细胞外基质物质的分解，从而使其过量积累。最终，小梁网途径和葡萄膜巩膜途径的房水流出减少，眼压升高，增加更多压力并使病理状况持续存在。未来的研究若能确定其他因素并阐明它们在这些过程中的作用，可能会为与年龄和青光眼相关的眼部变化带来替代疗法。
