青光眼视神经压力损伤相关分子机制研究进展

发布时间：2018-08-09 18:50

【摘要】：青光眼是一组具有特征性视神经损害及视野缺损,且以视网膜神经节细胞死亡为病理改变的疾病,是全球最常见的不可逆性致盲眼病。目前有关视神经损害的机制并不完全清楚,临床上亦缺乏有效的视神经保护治疗方法,尤其缺乏从分子水平提高视网膜神经节细胞对抗压力损害的干预方式。因此探讨视神经压力损伤的分子机制,比如经机械应力信号通路和炎性反应因素引起的视网膜继发性损伤机制等成为本领域研究热点。本文就上述研究进展进行综述。
[Abstract]:Glaucoma is a group of diseases with characteristic optic nerve damage and visual field defect and the death of retinal ganglion cells as the pathological change. Glaucoma is the most common irreversible blindness in the world. At present, the mechanism of optic nerve damage is not completely clear, and there is a lack of effective methods of optic nerve protection in clinic, especially the intervention of increasing retinal ganglion cells against pressure damage at molecular level. Therefore, exploring the molecular mechanism of optic nerve pressure injury, such as the mechanism of secondary retinal injury caused by mechanical stress signal pathway and inflammatory response factors, has become a hot topic in this field. This paper reviews the research progress mentioned above.
【作者单位】：中南大学爱尔眼科学院;首都医科大学附属北京同仁医院北京同仁眼科中心北京市眼科研究所眼科学与视觉科学北京市重点实验室;
【分类号】：R77

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