Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Laboratories for Neuroscience Research in Neurosurgery, Boston Children's Hospital, Boston, Massachusetts 02115, USA.
Annu Rev Vis Sci. 2020 Sep 15;6:195-213. doi: 10.1146/annurev-vision-022720-094953.
The damage or loss of retinal ganglion cells (RGCs) and their axons accounts for the visual functional defects observed after traumatic injury, in degenerative diseases such as glaucoma, or in compressive optic neuropathies such as from optic glioma. By using optic nerve crush injury models, recent studies have revealed the cellular and molecular logic behind the regenerative failure of injured RGC axons in adult mammals and suggested several strategies with translational potential. This review summarizes these findings and discusses challenges for developing clinically applicable neural repair strategies.
视网膜神经节细胞 (RGC) 及其轴突的损伤或丢失导致创伤后观察到的视觉功能缺陷，在退行性疾病（如青光眼）或压迫性视神经病变（如视神经胶质瘤）中也是如此。通过使用视神经挤压损伤模型，最近的研究揭示了成年哺乳动物损伤的 RGC 轴突再生失败的细胞和分子逻辑，并提出了几种具有转化潜力的策略。本综述总结了这些发现，并讨论了开发临床适用的神经修复策略所面临的挑战。
