上睑下垂
内质网
未折叠蛋白反应
细胞生物学
程序性细胞死亡
激酶
炎症体
高尔基体
蛋白激酶A
半胱氨酸蛋白酶12
半胱氨酸蛋白酶
医学
化学
细胞凋亡
免疫学
生物
生物化学
炎症
作者
Changsheng Yan,Yuan Ma,Li He,Jitao Cui,Xiaoyu Guo,Gang Wang,Liang Ji
标识
DOI:10.1016/j.intimp.2023.110293
摘要
The purpose of this study was to explore whether and how endoplasmic reticulum stress (ERS) could promote caspase-1-dependent pancreatic acinar cell pyroptosis via the protein kinase R-like ER kinase (PERK) pathway to aggravate acute pancreatitis (AP). Wistar rats and AR42J cells were used to establish the AP model. When indicated, ERS regulation was performed prior to AP induction,and genetic regulation was performed prior to ERS induction. First, we found that caspase-1-dependent pyroptosis and pyroptotic injury were regulated by ERS in AP. By regulating three pathways in the UPR, ERS promotes caspase-1-dependent pyroptosis and pyroptotic injury through the PERK pathway. To further validate that ERS promotes caspase-1-dependent pyroptosis and pyroptotic injury through PERK, we used the PERK inhibitor ISRIB. In conclusion, our results indicated that ERS exacerbates AP by promoting caspase-1-dependent pyroptosis via the PERK pathway.
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