High mobility group box 1 (HMGB1) is a key player in retinal inflammation. HMGB1 is a danger associated protein pattern receptor which can sense high glucose as a stressor. Increased HMGB1 levels have been found in patients with late stage diabetic retinopathy. HMGB1 can bind toll-like receptor 4 (TLR4) and the receptor for advanced glycation end-products (RAGE), leading to increased inflammation commonly through nuclear factor kappa beta (NFkB). Because diabetic patients have been found to have increased HMGB1 and RAGE levels, as well as polymorphisms of TLR4, a number of investigations have focused on inhibition of these pathways in the diabetic retina. Work in diabetic animal models and cell culture have demonstrated a number of factors that can inhibit HMGB1/TLR4/RAGE signaling. This regulation offers potential new avenues for therapeutic development. This review is focused on HMGB1 signaling and downstream pathways leading to inflammation in the diabetic retina.

高迁移率族框 1 (HMGB1) 是视网膜炎症的关键参与者。HMGB1 是一种危险相关的蛋白质模式受体，它可以将高葡萄糖感知为压力源。在晚期糖尿病视网膜病变患者中发现 HMGB1 水平升高。HMGB1 可以结合 toll 样受体 4 (TLR4) 和晚期糖基化终末产物 (RAGE) 受体，通常通过核因子κβ (NFkB) 导致炎症增加。因为已经发现糖尿病患者的 HMGB1 和 RAGE 水平增加，以及 TLR4 的多态性，许多研究都集中在糖尿病视网膜中这些途径的抑制上。在糖尿病动物模型和细胞培养中的工作已经证明了许多可以抑制 HMGB1/TLR4/RAGE 信号的因素。该法规为治疗开发提供了潜在的新途径。这篇综述的重点是 HMGB1 信号传导和导致糖尿病视网膜炎症的下游途径。