Grigsby Jeffery G, Cardona Sandra M, Pouw Cindy E, Muniz Alberto, Mendiola Andrew S, Tsin Andrew T C, Allen Donald M, Cardona Astrid E
Vision Health Specialties, 4109 N. Midland Drive, Midland, TX 79707, USA.
Department of Biology, The University of Texas at San Antonio, San Antonio, TX 78249, USA.
J Ophthalmol. 2014;2014:705783. doi: 10.1155/2014/705783. Epub 2014 Aug 31.
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.
越来越多的证据表明,慢性炎症在糖尿病视网膜病变的发生和发展中均起作用。也有证据表明,高血糖产生的分子可激活小胶质细胞。然而,作为中枢神经系统固有免疫细胞的小胶质细胞在糖尿病期间对视网膜组织损伤的确切作用仍不清楚。目前的数据表明,小胶质细胞反应失调与它们在几种与慢性炎症相关的神经疾病中的有害作用有关。随着炎性细胞因子和高血糖在糖尿病视网膜中扩散,小胶质细胞可转变为激活状态,数量增加,穿过视网膜迁移,自身成为炎性和凋亡分子的产生者,或者发挥抗炎作用。此外,小胶质细胞的基因变异可能是患者对糖尿病视网膜病变易感性中常见的一些个体差异的原因。