Nuclear eNOS Interacts With and S -Nitrosates ADAR1 to Modulate Type I Interferon Signaling and Endothelial Function

Our findings uncovered a novel mechanism linking nuclear eNOS-derived NO with the activity of ADAR1 to maintain vascular homeostasis. Reduced NO bioavailability results in previously unrecognized activation of a type I IFN response in the endothelium, which contributes to atherogenesis.