Loss of Smooth Muscle α-Actin Leads to NF-κB–Dependent Increased Sensitivity to Angiotensin II in Smooth Muscle Cells and Aortic Enlargement

Abstract

These findings reveal that disruption of smooth muscle α-actin filaments in smooth muscle cells increases reactive oxygen species levels, activates nuclear factor κB signaling, and increases AngII receptor type I a expression, thus potentiating AngII signaling in vascular smooth muscle cells without an increase in the exogenous levels of AngII.