Redox-dependent protein kinase regulation by angiotensin II: mechanistic insights and its pathophysiology

Abstract

Reactive oxygen species (ROS) are proposed to induce cardiovascular diseases, such as atherosclerosis, hypertension, restenosis, and fibrosis, through several mechanisms. One such mechanism involves ROS acting as intracellular second messengers, which lead to induction of unique signal transductions. Angiotensin II (AngII), a potent cardiovascular pathogen, stimulates ROS production through the G protein-coupled AngII type 1 receptor expressed in its target organs, such as vascular tissues, heart, and kidney. Recent accumulating evidence indicates that through ROS production, AngII activates downstream ROS-sensitive kinases that are critical in mediating cardiovascular remodeling. Each of these ROS-sensitive kinases could potentially mediate its own specific function. In this review, we will focus our discussion on the current findings that suggest novel mechanisms of how AngII mediates activation of these redox-sensitive kinases in target organs, as well as the pathological significance of their activation.