Cui Yongyong, Zhao Deming, Barrow Paul Andrew, Zhou Xiangmei
The State Key Lab of Agrobiotechnology, Key Lab of Animal Epidemiology and Zoonosis, Ministry of Agriculture, National TSE Lab, College of Veterinary Medicine, China Agricultural University, Beijing 100193, PR China.
School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, Loughborough, Leicestershire, UK.
Tuberculosis (Edinb). 2016 Mar;97:52-6. doi: 10.1016/j.tube.2015.12.009. Epub 2016 Jan 2.
Tuberculosis (TB) remains a major cause of mortality and morbidity in the worldwide. The endoplasmic-reticulum stress (ERS) response constitutes a cellular process that is triggered by mycobacterial infection that disturbs the folding of proteins in the endoplasmic reticulum (ER). The unfolded protein response (UPR) is induced to suspend the synthesis of early proteins and reduce the accumulation of unfolded- or misfolded proteins in the ER restoring normal physiological cell function. Prolonged or uncontrolled ERS leads to the activation of three signaling pathways (IRE1, PERK and ATF6) which directs the cell towards apoptosis. The absence of this process facilitates spread of the mycobacteria within the body. We summarize here recent advances in understanding the signaling pathway diversity governing ERS in relation to TB.
结核病（TB）仍是全球范围内主要的致死和致病原因。内质网应激（ERS）反应是一种细胞过程，由分枝杆菌感染引发，这种感染会干扰内质网（ER）中蛋白质的折叠。未折叠蛋白反应（UPR）被诱导，以暂停早期蛋白质的合成，并减少内质网中未折叠或错误折叠蛋白质的积累，从而恢复正常的细胞生理功能。长期或不受控制的ERS会导致三种信号通路（IRE1、PERK和ATF6）的激活，这会引导细胞走向凋亡。这个过程的缺失会促进分枝杆菌在体内的传播。我们在此总结了在理解与结核病相关的内质网应激信号通路多样性方面的最新进展。
