Zeng Menghao, Liang Guibin, Yuan Fangfang, Yan Shanshan, Liu Jie, He Zhihui
Department of Critical Care Medicine, the Third Xiangya Hospital, Central South University, Changsha, Hunan 410013, China.
Sepsis Translational Medicine Key Laboratory of Hunan Province, Changsha, Hunan, China.
iScience. 2024 Sep 20;27(10):110996. doi: 10.1016/j.isci.2024.110996. eCollection 2024 Oct 18.
Endothelial dysfunction is an important factor in the progress of sepsis. Endothelial progenitor cells (EPCs) are the precursor cells of endothelial cells and play a crucial role in the prognosis and treatment of sepsis. EPCs in the peripheral blood of patients with sepsis undergo pyroptosis, but the mechanism remains much of unknown. Serum high-mobility group box-1 (HMGB1) is significantly elevated in patients with sepsis, but whether it is related to EPCs pyroptosis is unknown. We used a cell model of sepsis to isolate EPCs for better observation. By detecting the pyroptosis-related indicators of EPCs and the level of release and acetylation of HMGB1 in inflammatory macrophages, it was found that HMGB1 released by inflammatory macrophages combined with receptor for advanced glycation end products (RAGE) is a key pathway to induce pyroptosis of EPCs.
内皮功能障碍是脓毒症进展中的一个重要因素。内皮祖细胞（EPCs）是内皮细胞的前体细胞，在脓毒症的预后和治疗中起关键作用。脓毒症患者外周血中的EPCs会发生焦亡，但其机制仍大多未知。脓毒症患者血清中的高迁移率族蛋白B1（HMGB1）显著升高，但它是否与EPCs焦亡有关尚不清楚。我们使用脓毒症细胞模型来分离EPCs以便更好地观察。通过检测EPCs的焦亡相关指标以及炎性巨噬细胞中HMGB1的释放水平和乙酰化水平，发现炎性巨噬细胞释放的HMGB1与晚期糖基化终末产物受体（RAGE）结合是诱导EPCs焦亡的关键途径。
