糖尿病对血-视网膜屏障超微结构影响的研究进展
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黑龙江省自然科学基金项目(No.D200949); 黑龙江省教育厅科学技术研究项目(No.11541219); 黑龙江省卫生厅科研项目(No.2007-222); 哈尔滨市科技局资助项目(No.2007RFQXS090)


Research progress of diabetes on the ultrastructure of blood retina barrier
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Natural Science Foundation of Heilongjiang Province, China(No.D200949); Science and Technology Department Project of Education Department, Heilongjiang Province, China(No.11541219); The Scientific Research Project of Health Department, Heilongjiang Province, China(No.2007-222); Harbin Science and Technology Fund, China(No.2007RFQXS090)

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    摘要:

    糖尿病视网膜病变(diabetic retinopathy,DR)是全世界最主要的致盲性眼病,也是最严重和最常见的微血管病变之一。糖尿病可造成血-视网膜屏障的损害引起血管源性水肿和神经组织损伤,造成视力下降。内层血-视网膜屏障主要是由视网膜毛细血管内皮细胞的紧密连接构成,此屏障阻碍血液的渗透及内源性物质和外源性物质在视网膜中的自由扩散,使视网膜保持恒定的环境,有效的供应营养物质。糖尿病患者的视网膜中由于细胞因子、生长因子、晚期糖基化终产物、炎症、高血糖症和周细胞丢失的增加,导致视网膜血管内皮细胞通透性增加。本文就糖尿病所引起的血-视网膜屏障超微结构改变进行综述。

    Abstract:

    Diabetic retinopathy is a major cause of blindness all over the world, and it is one of the most serious and common microvascular complications of diabetes. Breakdown of the endothelial blood-retinal barrier(BRB), as occurs in diabetic retinopathy, result in vasogenic edema and neural tissue damage, causing loss of vision. The inner BRB is created by complex tight juctions of retinal capillary endothelial cells, this barrier prevents the free diffusion of substances between the circulating blood and the neural retinal, the inner BRB efficiently supplies nutrients to the retinal and removes endobiotics and xenobiotics from the retina to maintain a constant milieu in the neural retina. The central mechanism of altered inner BRB function is a change in the permeability characteristics of retinal endothelial cells caused by elevated levels of cytokines, growth factors, advanced glycation end products, inflammation, hyperglycema and loss of pericytes. This article reviews the relationship between diabetes and the ultrastructure changes of BRB.

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周媛,崔浩,刘洪涛,等.糖尿病对血-视网膜屏障超微结构影响的研究进展.国际眼科杂志, 2014,14(7):1220-1222.

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  • 收稿日期:2014-03-11
  • 最后修改日期:2014-06-11
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  • 在线发布日期: 2014-06-19
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