發(fā)布時間：2018-08-09 18:50

【摘要】：青光眼是一組具有特征性視神經(jīng)損害及視野缺損,且以視網(wǎng)膜神經(jīng)節(jié)細胞死亡為病理改變的疾病,是全球最常見的不可逆性致盲眼病。目前有關視神經(jīng)損害的機制并不完全清楚,臨床上亦缺乏有效的視神經(jīng)保護治療方法,尤其缺乏從分子水平提高視網(wǎng)膜神經(jīng)節(jié)細胞對抗壓力損害的干預方式。因此探討視神經(jīng)壓力損傷的分子機制,比如經(jīng)機械應力信號通路和炎性反應因素引起的視網(wǎng)膜繼發(fā)性損傷機制等成為本領域研究熱點。本文就上述研究進展進行綜述。
[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.
【作者單位】： 中南大學愛爾眼科學院;首都醫(yī)科大學附屬北京同仁醫(yī)院北京同仁眼科中心北京市眼科研究所眼科學與視覺科學北京市重點實驗室;
【分類號】：R77

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1 張和武;靖秋生;;乙胺丁醇的視神經(jīng)損害[A];中國防癆協(xié)會臨床委員會、中國防癆協(xié)會基礎委員會學術研討會論文集[C];2008年

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