Endothelial cell-specific reactive oxygen species production increases susceptibility to aortic dissection.

ABSTRACT:

Background

Increased production of reactive oxygen species (ROS) throughout the vascular wall is a feature of cardiovascular disease states, but therapeutic strategies remain limited by our incomplete understanding of the role and contribution of specific vascular cell ROS to disease pathogenesis. To investigate the specific role of endothelial cell (EC) ROS in the development of structural vascular disease, we generated a mouse model of endothelium-specific Nox2 overexpression and tested the susceptibility to aortic dissection after angiotensin II (Ang II) infusion.

Methods and results

A specific increase in endothelial ROS production in Nox2 transgenic mice was sufficient to cause Ang II-mediated aortic dissection, which was never observed in wild-type mice. Nox2 transgeni

SUBMITTER: Fan LM 

PROVIDER: S-EPMC5357047 | biostudies-literature | 2014 Jun

REPOSITORIES: biostudies-literature