Knockdown of sestrin2 increases pro-inflammatory reactions and ER stress in the endothelium via an AMPK dependent mechanism

Article ID	Journal	Published Year	Pages	File Type
5501046	Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease	2017	33 Pages	PDF

Abstract

Knockdown of sesn2 aggravates atherosclerotic processes by increasing pro-inflammatory reactions and ER stress in the endothelium via an AMPK-dependent mechanism, suggesting that sesn2 might be a novel therapeutic target for atherosclerosis.

Keywords

MCP-1 NF-κB TNFα HUVEC ICAM-1 LPS IL-6 Sesn2 Sestrin2 AMPK AMP-activated protein kinase ROS Atherosclerosis ER stress Endothelium interleukin 6 tumor necrosis factor alpha Human umbilical vein endothelial cells endoplasmic reticulum nuclear factor kappa B lipopolysaccharide Intercellular adhesion molecule 1 Vascular cell adhesion molecule 1 monocyte chemoattractant protein 1 Reactive oxygen species

Related Topics

Life Sciences Biochemistry, Genetics and Molecular Biology Ageing

Preview

Knockdown of sestrin2 increases pro-inflammatory reactions and ER stress in the endothelium via an AMPK dependent mechanism

Authors

Hwan-Jin Hwang, Tae Woo Jung, Ju-Hee Choi, Hyun Jung Lee, Hye Soo Chung, Ji A Seo, Sin Gon Kim, Nan Hee Kim, Kyung Mook Choi, Dong Seop Choi, Sei Hyun Baik, Hye Jin Yoo,