Related Experiment Video
Updated: Feb 10, 2026

Activating Autophagy by Aerobic Exercise in Mice
Published on: February 3, 2017
Glucocorticoid-activated IRE1α/XBP-1s signaling: an autophagy-associated protective pathway against endotheliocyte
Yanchun Gao1, Hongyi Zhu1, Fan Yang1
1Department of Orthopedic Surgery, Shanghai Jiaotong University Affiliated Sixth People's Hospital , Shanghai , China.
Abstract:
Glucocorticoid-induced endothelial injury has been reported in several diseases. Although there are several theories, the exact mechanism underlying the role of glucocorticoids in this process remains unclear. Autophagy has been reported to occur as a response to different stimuli and can affect cell survival and function. In this study, we found that glucocorticoids induced apoptosis and endoplasmic reticulum (ER) stress in endotheliocytes. Furthermore, we discovered that glucocorticoids induced autophagy in these cells and the inositol requiring protein 1 (IRE1α)/X-box binding protein 1s (XBP-1s) axis, one of the downstream signaling pathways of ER stress, was associated with the glucocorticoid-induced autophagy. The autophagy partly protected endotheliocytes from glucocorticoid-induced apoptosis and inhibition of proliferation. In conclusion, glucocorticoid-induced endoplasmic reticulum stress activated the IRE1α/XBP-1s signaling and induced autophagy, which, in turn, played a protective role in endotheliocyte survival and proliferation, avoiding further cellular damage caused by glucocorticoids.
Insights
Glucocorticoids cause endoplasmic reticulum stress and autophagy in endotheliocytes. This autophagy, activated by the IRE1α/XBP-1s pathway, protects cells from glucocorticoid-induced damage and apoptosis.
Area of Science:
- Cell Biology
- Molecular Biology
- Pathology
Background:
- Glucocorticoid-induced endothelial injury is a recognized phenomenon in various diseases.
- The precise molecular mechanisms linking glucocorticoids to endothelial dysfunction remain incompletely understood.
- Autophagy is a cellular process involved in stress response and cell survival.
Purpose of the Study:
- To elucidate the role of autophagy in glucocorticoid-induced endotheliocyte injury.
- To investigate the signaling pathways involved in glucocorticoid-induced autophagy.
- To determine the functional consequences of autophagy in endotheliocytes under glucocorticoid exposure.
Main Methods:
- Treatment of endotheliocytes with glucocorticoids.
- Assessment of apoptosis and endoplasmic reticulum (ER) stress.
- Analysis of autophagy induction and the involvement of the IRE1α/XBP-1s pathway.
- Evaluation of cell proliferation and survival.
Main Results:
- Glucocorticoids induced apoptosis and ER stress in endotheliocytes.
- Glucocorticoids stimulated autophagy, which was linked to the IRE1α/XBP-1s signaling pathway.
- Autophagy partially protected endotheliocytes from glucocorticoid-induced apoptosis and proliferation inhibition.
Conclusions:
- Glucocorticoid-induced ER stress activates the IRE1α/XBP-1s pathway, leading to autophagy.
- Autophagy plays a protective role in endotheliocyte survival and proliferation against glucocorticoid-induced damage.
Related Concept Videos
Notch Signaling Pathway
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not...
Hedgehog Signaling Pathway
Interactions Between Signaling Pathways
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
Non-Canonical Wnt Signaling Pathways
Canonical Wnt Signaling Pathway
NF-κB-dependent Signaling Pathway
NF-κB-dependent Signaling Mechanism
The...

