Review Article, J Pharmacol Biomed Anal Vol: 1 Issue: 2
Endoplasmic Reticulum Stress and Related Pathological Processes
| Yu Mei, Melissa D Thompson, Richard A Cohen and XiaoYong Tong* |
| Vascular Biology Section, Boston University School of Medicine, Boston, Massachusetts 02118, USA |
| Corresponding author : XiaoYong Tong Vascular Biology Section, Boston University, School of Medicine, 650 Albany Street, X729, Boston, MA, 02118, USA E-mail: xytong@bu.edu |
| Received: October 16, 2012 Accepted: November 08, 2013 Published: November 15, 2013 |
| Citation: Mei Y, Thompson MD, Cohen RA, Tong XY (2013) Endoplasmic Reticulum Stress and Related Pathological Processes. J Pharmacol Biomed Anal 1:2. doi:10.4172/2327-4638.1000105 |
Abstract
Endoplasmic Reticulum Stress and Related Pathological Processes
The endoplasmic reticulum (ER) plays a pivotal role in lipid and protein biosynthesis as well as calcium store regulation, which determines its essential role in cell function. Hypoxia, nutrient deprivation, perturbation of redox status and aberrant calcium regulation can all trigger the ER stress response, which is mediated through three main sensors, namely inositol requiring element-1 (IRE-1), protein kinase-like ER kinase (PERK) and activating transcription factor 6 (ATF6). This review explores the interaction of ER stress and ER stress-associated pathological processes, including inflammation, apoptosis, aberrant autophagy, mitochondrial dysfunction and hypoxic responses. In addition, the correlation of ER stress with lipid and calcium homeostasis and dysregulation, and its role in disease development is also presented. Improved understanding of ER stress and its cofactors in pathological processes may provide new perspective on disease development and control.
