Department of Ophthalmology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Department of Orthopedics, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Front Immunol. 2023 Apr 25;14:1151185. doi: 10.3389/fimmu.2023.1151185. eCollection 2023.
In the working-age population worldwide, diabetic retinopathy (DR), a prevalent complication of diabetes, is the main cause of vision impairment. Chronic low-grade inflammation plays an essential role in DR development. Recently, concerning the pathogenesis of DR, the Nod-Like Receptor Family Pyrin Domain Containing 3 (NLRP3) inflammasome in retinal cells has been determined as a causal factor. In the diabetic eye, the NLRP3 inflammasome is activated by several pathways (such as ROS and ATP). The activation of NPRP3 leads to the secretion of inflammatory cytokines interleukin-1β (IL-1β) and interleukin-18 (IL-18), and leads to pyroptosis, a rapid inflammatory form of lytic programmed cell death (PCD). Cells that undergo pyroptosis swell and rapture, releasing more inflammatory factors and accelerating DR progression. This review focuses on the mechanisms that activate NLRP3 inflammasome and pyroptosis leading to DR. The present research highlighted some inhibitors of NLRP3/pyroptosis pathways and novel therapeutic measures concerning DR treatment.
在全球劳动年龄人群中，糖尿病视网膜病变（DR）是糖尿病的一种常见并发症，也是导致视力损害的主要原因。慢性低度炎症在 DR 的发展中起着至关重要的作用。最近，在研究 DR 的发病机制时，人们发现视网膜细胞中的 Nod-Like Receptor Family Pyrin Domain Containing 3（NLRP3）炎性小体是一个致病因素。在糖尿病眼中，NLRP3 炎性小体可通过多种途径（如 ROS 和 ATP）被激活。NPRP3 的激活会导致促炎细胞因子白细胞介素-1β（IL-1β）和白细胞介素-18（IL-18）的分泌，并导致细胞发生细胞焦亡，这是一种快速炎症形式的细胞程序性死亡（PCD）。发生细胞焦亡的细胞会肿胀和破裂，释放更多的炎症因子，从而加速 DR 的进展。本综述重点介绍了激活 NLRP3 炎性小体和细胞焦亡导致 DR 的机制。目前的研究强调了一些 NLRP3/细胞焦亡途径的抑制剂以及针对 DR 治疗的新的治疗措施。
