Endoplasmic Reticulum Stress-apoptosis Pathways And Post-traumatic Stress Disorder
The endoplasmic reticulum(ER),as an important organelle for protein synthesis,plays an important role in maintaining cellular homeostasis.In order to ensure the normal operation of endoplasmic reticulum function at the beginning of endoplasmic reticu-lum stress,an unfolded protein reaction is initiated to maintain cell survival in vivo,but when there are too many unfolded or misfolded proteins,apoptosis will be induced.There is growing evidence that endoplasmic reticulum stress-mediated apoptosis pathways play a critical role in all pathological stages of PTSD.Oxidative stress,calcium homeostasis imbalance and inflammatory response,as the main pathological factors leading to endoplasmic reticulum dysfunction,are also widely involved in the pathogenesis of post-traumatic stress disorder.Endoplasmic reticulum stress initiates the non-folding protein reaction and initiates the apoptosis pathway by activating the three endoplasmic reticulum pathways PERK,IRE1 and ATF6.Reducing the apoptosis rate of nerve cells by regulating the endo-plasmic reticulum stress-apoptosis pathway or inhibiting the expression of key proteins of related pathways may provide new therapeutic targets for the treatment of post-traumatic stress disorder.The specific mechanism of endoplasmic reticulum stress-apoptosis pathway in PTSD needs to be further explored,and this pathway will help to develop new drugs and treatment strategies for PTSD.