A review of the effects of 17 β-estradiol on endoplasmic reticulum stress: mechanisms and pathway

The endoplasmic reticulum (ER) is an important organelle responsible for protein folding, calcium homeostasis and lipid biosynthesis. Accumulation of unfolded or misfolded proteins by hypoxia, loss of Ca2+ homeostasis and nutrient deprivation leads to endoplasmic reticulum stress (ERS) and then the unfolded protein response (UPR) is activated as a defense mechanism to restore endoplasmic reticulum homeostasis. It is now known that the ERS and the UPR are implicated in a variety of diseases such as diabetes, inflammatory diseases, neurodegenerative diseases and osteoporosis. Steroid hormones such as 17-βestradiol have been extensively reported to possess beneficial effects in different diseases. In this article, the concept of ERS, the underlying molecular mechanisms, and their relationship to several pathological conditions and finally, the role of 17-βestradiol and its receptors in moderating ERS and UPR are discussed to provide theoretical basis for in-depth study.