Abstract
Background:Oxidative stress is critical for the fibrotic response of mesangial cells (MCs) to angiotensin II. Results:Nox4- and mitochondrial reactive oxygen species (ROS)-dependent endothelial nitric-oxide synthase (eNOS) uncoupling led to fibronectin accumulation in MCs stimulated by angiotensin II. Conclusion:The Nox4/mitochondrial ROS/eNOS pathway mediates angiotensin II-induced MC injury. Significance:Targeting Nox4 and mitochondrial ROS is a promising therapeutic approach.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 28668-28686 |
| Number of pages | 19 |
| Journal | Journal of Biological Chemistry |
| Volume | 288 |
| Issue number | 40 |
| DOIs | |
| State | Published - Oct 4 2013 |
ASJC Scopus subject areas
- Biochemistry
- Molecular Biology
- Cell Biology