Host: The Japanese Society of Toxicology
Salubrinal sustained phosphorylation of eIF2α and regulate cell death, but the mechanism is not clear. In this study, salubrinal significantly prevented the CdCl2 induced cell death. ER stress/autophagy were responsed by CdCl2, and further elevated by co-treatment with salubrinal. The mechanism is that salubrinal sustained phosphorylation of eIF2α, resulting in a simultaneous response to ER stress and autophagy, but the CdCl2 induced CHOP mRNAs were suppressed by salubrinal, which may have prevented cell death. These results recently reported the cooperation of ER stress response and autophagy.