Published in Gene Therapy Weekly, June 12th, 2008
"We hypothesized that Ang II could induce mitochondrial oxidative damage that in turn might decrease endothelial nitric oxide (NO center dot) bioavailability and promote vascular oxidative stress. The effect of Ang II on mitochondrial ROS, mitochondrial respiration, membrane potential, glutathione, and endothelial NO center dot was studied in isolated mitochondria and intact bovine aortic endothelial cells...
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