摘要
急性胰腺炎(acute pancreatitis, AP)作为临床常见的急腹症,以胰蛋白酶过度激活引发的腺泡细胞及周围组织自身消化为主要特征。大量证据表明,持续钙超载导致腺泡细胞坏死及过度凋亡是AP的重要发病环节。钙库操纵的Ca^(2+)通道(store-operated calcium entry, SOCE)是引起包括胰腺腺泡细胞在内的非兴奋细胞钙超载的关键,而钙释放激活钙通道蛋白Orai作为SOCE信号通路的核心分子调节钙通道的开放状态。新近的研究证实,SOCE通路在调控胰腺腺泡细胞钙超载上发挥重要作用。该文拟对SOCE调控钙超载参与AP的研究进展做一综述。
Acute pancreatitis is an inflammatory, multifactorial disease of the pancreas, resulting in mistargeting of digestive enzymes that eventually destroy the pancreatic parenchyma. It is now well established that persistent calcium overload-induced acinar cell necrosis and excessive apoptosis is an important pathogenesis of AP. The store-operated calcium entry(SOCE) is the key to cause calcium overload in non-excited cells, including pancreatic acinar cells, and calcium release activates calcium channel protein Orai as a core molecule in the SOCE signaling pathway. Recent studies have confirmed that the SOCE pathway plays an important role in regulating calcium overload in pancreatic acinar cells. This article is intended to review the progress of SOCE in regulating calcium overload in AP.
作者
段丽芳
张红
DUAN Li-Fang;ZHANG Hong(Basic Medical College,Shaanxi University of Chinese Medicine,Xianyang 712046,China)
出处
《生命科学》
CSCD
北大核心
2019年第2期160-165,共6页
Chinese Bulletin of Life Sciences
基金
国家自然科学基金项目(81603420)
陕西省科技厅自然科学基础研究计划(2017JM8076)
