Zhang Xiaoliang, Xu Chenchen, Ji LiJuan, Zhang Haiwei
Department of Gastroenterology, Weifang People's Hospital, Weifang, Shandong, China.
Department of Pediatrics, Weifang People's Hospital, Weifang, Shandong, China.
Cell Stress Chaperones. 2025 May;30(3):119-129. doi: 10.1016/j.cstres.2025.03.001. Epub 2025 Mar 17.
Acute pancreatitis (AP) is associated with multiple cellular mechanisms that trigger and or are triggered by the inflammatory injury and death of the acinar cells. One of the key mechanisms is the endoplasmic reticulum (ER) stress, which manifests as an accumulation of misfolded proteins within ER, an event that has proinflammatory and proapoptotic consequences. Hence, the degree of cell insult during AP could considerably depend on the signaling pathways that are upregulated during ER stress and its resulting dyshomeostasis such as C/EBP homologous protein (CHOP), cJUN NH2-terminal kinase (JNK), nuclear factor kappa B (NF-κB), and NOD-like receptor protein 3 (NLRP3) inflammasome. Exploring these molecular pathways is an interesting area for translational medicine as it may lead to identifying new therapeutic targets in AP. This review of the literature aims to shed light on the different roles of ER stress in the etiopathogenesis and pathogenesis of AP. Then, it specifically focuses on the therapeutic implications of ER stress in this context.
急性胰腺炎（AP）与多种细胞机制相关，这些机制引发腺泡细胞的炎症性损伤和死亡，或由其触发。关键机制之一是内质网（ER）应激，表现为内质网内错误折叠蛋白的积累，这一事件具有促炎和促凋亡的后果。因此，AP期间细胞损伤的程度在很大程度上可能取决于内质网应激期间上调的信号通路及其导致的内稳态失调，如C/EBP同源蛋白（CHOP）、c-JUN氨基末端激酶（JNK）、核因子κB（NF-κB）和NOD样受体蛋白3（NLRP3）炎性小体。探索这些分子途径是转化医学中一个有趣的领域，因为这可能会在AP中确定新的治疗靶点。这篇文献综述旨在阐明内质网应激在AP的病因发病机制和发病机制中的不同作用。然后，它特别关注内质网应激在这种情况下的治疗意义。
