内质网应激介导的胰岛β细胞凋亡研究进展

Progress on Islet β Cells Apoptosis Mediated by Endoplasmic Reticulum Stress

胰岛β细胞具有十分发达的内质网(ER),并且对应激非常敏感。多种原因都会使ER的稳态被破坏,引起未折叠蛋白反应(UPR)以及Ca^2+稳态失衡,进一步诱发内质网应激(ERS)。适度的ERS有利于恢复其稳态,过度的ERS会导致ER功能受损,并进一步诱导胰岛β细胞凋亡,从而介导糖尿病的发生、发展。因此,对生理及病理条件引发的ERS进行分析,探讨ERS介导的胰岛β细胞凋亡,可为糖尿病的深入研究奠定理论基础。

Islet cells have highly developed endoplasmic reticulum (ER) and are very sensitive to stress.The stable state of ER is destroyed for various reasons,causing Unfoldable protein reaction (UPR) and Ca^2+ steady-state imbalance, and further inducing endoplasmic reticulum stress (ERS).The moderate ERS is conducive to restoring its homeostasis,while excessive ERS will lead to impaire ER function and further induce apoptosis of islet neurons,thus mediating the occurrence and development of diabetes.Therefore,the physiological and pathological conditions of ERS were analyzed,and the apoptosis of the islet XPS cells induced by ERS was discussed,laying a theoretical foundation for the in-depth study of diabetes.