Department of Ophthalmology & Visual Sciences, University of Louisville, Louisville, KY, USA.
Exp Eye Res. 2011 Aug;93(2):178-86. doi: 10.1016/j.exer.2010.07.009. Epub 2010 Aug 13.
Neurodegenerative insults and glial activation during glaucomatous neurodegeneration initiate an immune response to restore tissue homeostasis and facilitate tissue cleaning and healing. However, increasing risk factors over a chronic and cumulative period may lead to a failure in the regulation of innate and adaptive immune response pathways and represent a route for conversion of the beneficial immunity into a neuroinflammatory degenerative process contributing to disease progression. Oxidative stress developing through the pathogenic cellular processes of glaucoma, along with the aging-related component of oxidative stress, likely plays a critical role in shifting the physiological equilibrium. This review aims to provide a perspective on the complex interplay of cellular events during glaucomatous neurodegeneration by proposing a unifying scheme that integrates oxidative stress-related risk factors with the altered regulation of immune response in glaucoma.
神经退行性损伤和神经胶质细胞激活在青光眼神经退行性变过程中引发免疫反应,以恢复组织内稳态并促进组织清洁和修复。然而,在慢性和累积的时间段内,风险因素的增加可能导致先天和适应性免疫反应途径的调节失败,并代表将有益免疫转化为神经炎症退行性过程的途径,从而导致疾病进展。通过青光眼的致病细胞过程发展起来的氧化应激,以及与氧化应激相关的衰老成分,可能在改变生理平衡方面发挥关键作用。本综述旨在通过提出一个统一的方案,将与氧化应激相关的风险因素与青光眼免疫反应的改变调节结合起来,为青光眼神经退行性变过程中细胞事件的复杂相互作用提供一个视角。