The Role of Microglia in Diabetic Retinopathy

被引:168
作者
Grigsby, Jeffery G. [1 ]
Cardona, Sandra M. [2 ]
Pouw, Cindy E. [3 ]
Muniz, Alberto [2 ]
Mendiola, Andrew S. [2 ]
Tsin, Andrew T. C. [2 ]
Allen, Donald M. [4 ]
Cardona, Astrid E. [2 ]
机构
[1] Vis Hlth Specialties, Midland, TX 79707 USA
[2] Univ Texas San Antonio, Dept Biol, San Antonio, TX 78249 USA
[3] Univ Houston, Coll Optometry, Houston, TX 77204 USA
[4] Univ Texas Permian Basin, Dept Biol, Odessa, TX 79762 USA
基金
美国国家卫生研究院;
关键词
ADVANCED GLYCATION ENDPRODUCTS; ENDOTHELIAL GROWTH-FACTOR; NITRIC-OXIDE SYNTHASE; ALPHA TNF-ALPHA; RETINAL MICROGLIA; CONTRAST SENSITIVITY; OXIDATIVE STRESS; END-PRODUCTS; MOUSE MODEL; MICROVASCULAR COMPLICATIONS;
D O I
10.1155/2014/705783
中图分类号
R77 [眼科学];
学科分类号
100212 ;
摘要
There is growing evidence that chronic inflammation plays a role in both the development and progression of diabetic retinopathy. There is also evidence that molecules produced as a result of hyperglycemia can activate microglia. However the exact contribution of microglia, the resident immune cells of the central nervous system, to retinal tissue damage during diabetes remains unclear. Current data suggest that dysregulated microglial responses are linked to their deleterious effects in several neurological diseases associated with chronic inflammation. As inflammatory cytokines and hyperglycemia disseminate through the diabetic retina, microglia can change to an activated state, increase in number, translocate through the retina, and themselves become the producers of inflammatory and apoptotic molecules or alternatively exert anti-inflammatory effects. In addition, microglial genetic variations may account for some of the individual differences commonly seen in patient's susceptibility to diabetic retinopathy.
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页数:15
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