Lebrun-Julien Frédéric, Di Polo Adriana
Department of Pathology, Université de Montréal, Montreal, Quebec, Canada.
Optom Vis Sci. 2008 Jun;85(6):417-24. doi: 10.1097/OPX.0b013e31817841f7.
A hallmark of glaucomatous optic nerve damage is retinal ganglion cell (RGC) death. RGCs, like other central nervous system neurons, have a limited capacity to survive or regenerate an axon after injury. Strategies that prevent or slow down RGC degeneration, in combination with intraocular pressure management, may be beneficial to preserve vision in glaucoma. Recent progress in neurobiological research has led to a better understanding of the molecular pathways that regulate the survival of injured RGCs. Here we discuss a variety of experimental strategies including intraocular delivery of neuroprotective molecules, viral-mediated gene transfer, cell implants and stem cell therapies, which share the ultimate goal of promoting RGC survival after optic nerve damage. The challenge now is to assess how this wealth of knowledge can be translated into viable therapies for the treatment of glaucoma and other optic neuropathies.
青光眼性视神经损伤的一个标志是视网膜神经节细胞（RGC）死亡。RGC与其他中枢神经系统神经元一样，受伤后存活或再生轴突的能力有限。预防或减缓RGC变性的策略，与眼压管理相结合，可能有助于保护青光眼患者的视力。神经生物学研究的最新进展使人们对调节受损RGC存活的分子途径有了更好的理解。在这里，我们讨论了各种实验策略，包括眼内递送神经保护分子、病毒介导的基因转移、细胞植入和干细胞疗法，这些策略的最终目标都是促进视神经损伤后RGC的存活。现在面临的挑战是评估如何将这些丰富的知识转化为治疗青光眼和其他视神经病变的可行疗法。
