α1AMP-Activated Protein Kinase Preserves Endothelial Function During Chronic Angiotensin II Treatment by Limiting Nox2 Upregulation

Abstract

Our data indicate that in vivo α1AMPK deletion leads to Nox2 upregulation, resulting in endothelial dysfunction and vascular inflammation. This implicates basal AMPK activity as a protective, redox-regulating element in vascular homeostasis.