小胶质细胞在糖尿病视网膜病变中的作用
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国家自然科学基金面上项目(No.81570852); 上海申康医院发展中心临床科技创新项目(No.SHDC12016116); 上海交通大学医学院附属仁济医院临床科研创新培育基金(No.PYIII-17-030)


Function of microglia in diabetic retinopathy
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National Natural Science Foundation of China(No.81570852); Shanghai Shenkang Hospital Development Center's Clinical Science and Technology Innovation Project(No.SHDC12016116); Renji Hospital, Shanghai Jiao Tong University School of Medicine,Clinical Research Innovation and Cultivation Foundation(No.PYIII-17-030)

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    摘要:

    糖尿病视网膜病变(DR)作为糖尿病最常见的并发症之一,是世界范围内工作人群主要的致盲疾病。DR曾被认为是视网膜微血管病变。随着研究的不断深入,视网膜神经元病变和中低度炎症也被证实是DR的重要发病机制。小胶质细胞是视网膜内的常驻巨噬细胞,主要分布在内层视网膜,负责监控视网膜内微环境变化。在异常刺激下,小胶质细胞活化并与视网膜内不同类型的细胞发生复杂的相互作用。在DR中,小胶质细胞被激活,活化的小胶质细胞内关键因子或多条通路被激活,产生大量的炎症因子、趋化因子等。同时,活化的小胶质细胞增殖能力及迁移增强,外层视网膜内小胶质细胞数量增多。小胶质细胞的过度活化最终引起视网膜神经元凋亡、血-视网膜屏障破坏,导致视力丢失。

    Abstract:

    Diabetic retinopathy(DR), one of the most common complications of diabetes mellitus, is the leading cause of blindness in working-age population. DR, previously regarded as a microvascular disease, is also considered as neuronopathy and low-to-moderate inflammation in retina with research progression. Microglias, the resident macrophage in the inner retina, are responsible for surveillance of the microenvironment in retina. Under abnormal conditions, microglias are activated and interact with different types of cells in retina. In DR, microglias become activated, as evidenced by the activation of the key molecules or signal transduction pathways, such as the nuclear factor kappa-light-chain-enhancer of activated B cells(NF-κB)and extracellular signal-regulated kinase(ERK)signaling pathways, which lead to the increased production of pro-inflammatory factors, chemokines, etc. At the same time, the proliferation and migration of activated microglia are enhanced, and microglias migrate to the outer retina. The over-activation of microglias causes neuronal cell apoptosis and blood-retinal barrier breakdown, resulting in vision loss.

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易秋雪,张敬法,柳林.小胶质细胞在糖尿病视网膜病变中的作用.国际眼科杂志, 2019,19(12):2048-2052.

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  • 收稿日期:2019-05-05
  • 最后修改日期:2019-10-31
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  • 在线发布日期: 2019-11-21
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