Laboratory for Experimental Immunology of the Eye, Department of Ophthalmology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
Center for Molecular Medicine, University of Cologne, Cologne, Germany.
Front Immunol. 2020 Nov 6;11:564077. doi: 10.3389/fimmu.2020.564077. eCollection 2020.
Diabetic retinopathy is a vision-threatening disease affecting neurons and microvasculature of the retina. The development of this disease is associated with the action of inflammatory factors that are connected to the activation of microglial cells, the resident tissue macrophages of the CNS. In the quiescent state, microglial cells help maintain tissue homeostasis in the retina through phagocytosis and control of low-grade inflammation. However, prolonged tissue stress due to hyperglycemia primes microglia to become overly reactive with the concomitant production of pro-inflammatory cytokines and chemokines causing chronic inflammation. In this review, we provide evidence of microglial cell activation and pro-inflammatory molecules associated with the development and progression of diabetic retinopathy. We further highlight innovative animal models that can mimic the disease in humans and discuss strategies in modulating microglial-mediated inflammation as potential therapeutic approaches in managing the disease.
糖尿病性视网膜病变是一种威胁视力的疾病，影响视网膜的神经元和微血管。这种疾病的发展与炎症因子的作用有关，炎症因子与小胶质细胞的激活有关，小胶质细胞是中枢神经系统的固有组织巨噬细胞。在静止状态下，小胶质细胞通过吞噬作用和控制低度炎症来帮助维持视网膜的组织内稳态。然而，由于高血糖引起的组织长期应激使小胶质细胞变得过度活跃，同时产生促炎细胞因子和趋化因子，导致慢性炎症。在这篇综述中，我们提供了小胶质细胞激活和与糖尿病性视网膜病变发展和进展相关的促炎分子的证据。我们进一步强调了可以模拟人类疾病的创新动物模型，并讨论了调节小胶质细胞介导的炎症作为管理该疾病的潜在治疗方法的策略。
