Abstract
The oxidation of LDLs is considered a key step in the development of atherosclerosis. How LDL oxidation contributes to atherosclerosis remains poorly defined. Here we report that oxidized and glycated LDL (HOG-LDL) causes aberrant endoplasmic reticulum (ER) stress and that the AMP-activated protein kinase (AMPK) suppressed HOG-LDL-triggered ER stress in vivo.
| Original language | English |
|---|---|
| Pages (from-to) | 1386-96 |
| Number of pages | 11 |
| Journal | Diabetes |
| Volume | 59 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - Jun 2010 |
Keywords
- AMP-Activated Protein Kinases
- Animals
- Aorta
- Apolipoproteins E
- Cattle
- Crosses, Genetic
- Endoplasmic Reticulum
- Endothelium, Vascular
- Enzyme Activation
- Gene Expression Regulation
- Humans
- Lipoproteins, LDL
- Mice
- Mice, Inbred C57BL
- Mice, Knockout
- RNA, Small Interfering
- Umbilical Veins
Fingerprint
Dive into the research topics of 'Activation of AMP-activated protein kinase inhibits oxidized LDL-triggered endoplasmic reticulum stress in vivo'. Together they form a unique fingerprint.Cite this
- APA
- Author
- BIBTEX
- Harvard
- Standard
- RIS
- Vancouver