Endoplasmic reticulum stress and vascular endothelial cell apoptosis.
10.3881/j.issn.1000-503X.2014.01.019
- Author:
Zhi-ling QIU
1
;
Jun-ping ZHANG
2
;
Xiao-chen GUO
2
Author Information
1. Graduate School, the First Affiliated Hospital, Tianjin University of Chinese Medicine, Tianjin 300193, China.
2. Department of Cardiovascular, the First Affiliated Hospital, Tianjin University of Chinese Medicine, Tianjin 300193, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Apoptosis;
Endoplasmic Reticulum Stress;
Endothelial Cells;
pathology;
Humans
- From:
Acta Academiae Medicinae Sinicae
2014;36(1):102-107
- CountryChina
- Language:Chinese
-
Abstract:
Endoplasmic reticulum stress (ERS) is a new pathway of apoptosis following the discovery of death receptor signaling pathway and mitochondrial pathway. By activating the unfolded protein response (UPR), ERS can suspend protein synthesis, restore the endoplasmic reticulum homeostasis, and thus play a protective role for cells; however, if the inducing factors of ERS persist, ERS will continue to trigger C/EBP homologous protein, JNK, caspase, or other pathways to induce apoptosis. In addition, the injury and apoptosis of vascular endothelial cells are key links in various diseases and pathophysiologic processes, and research has also shown that vascular endothelial cell apoptosis is closely related with the ERS. Effective intervention of ERS may restrain apoptosis and protect the vascular endothelium. This article reviews the recent research advances in ERS and its role in vascular endothelial cell apoptosis.
