Neuropharmacology and Neurobiology Section, University of Birmingham, Birmingham, United Kingdom.
Invest Ophthalmol Vis Sci. 2012 May 17;53(6):2913-20. doi: 10.1167/iovs.11-8564.
Retinal injury is a common cause of profound and intractable loss of vision. Clinical outcomes are poor in both open and closed globe injuries because cell death, scarring, and a failure of tissue and axon regeneration are not ameliorated by current treatments. Much animal research is directed at understanding and modifying these pathologies, although results have yet to translate into clinical practice. Axotomy-induced retinal ganglion cell (RGC) death in mammals can be effectively reduced and axon regeneration enhanced over the short term. After retinal injury in mammals, the retinal pigment epithelium (RPE) and retinal glia either regenerate lost RPE and neuroretinal cells or form nonfunctional scars. An understanding of the mechanisms underlying injury responses is critical to the successful development of therapeutic strategies to promote ocular repair.
视网膜损伤是导致严重且难以治愈的视力丧失的常见原因。开放性和闭合性眼球损伤的临床结果都较差,因为目前的治疗方法并不能减轻细胞死亡、瘢痕形成以及组织和轴突再生失败。尽管动物研究的结果尚未转化为临床实践,但许多动物研究都致力于理解和改变这些病理。在哺乳动物中,轴突切断诱导的视网膜神经节细胞 (RGC) 死亡可以在短期内得到有效减少,轴突再生也可以得到增强。在哺乳动物的视网膜损伤后,视网膜色素上皮 (RPE) 和视网膜神经胶质细胞要么再生失去的 RPE 和神经视网膜细胞,要么形成无功能的瘢痕。了解损伤反应的机制对于成功开发促进眼部修复的治疗策略至关重要。