G Protein–Dependent and G Protein–Independent Signaling Pathways and Their Impact on Cardiac Function

Abstract

G protein-coupled receptors signal through a variety of mechanisms that impact cardiac function, including contractility and hypertrophy. G protein–dependent and G protein–independent pathways each have the capacity to initiate numerous intracellular signaling cascades to mediate these effects. G protein–dependent signaling has been studied for decades and great strides continue to be made in defining the intricate pathways and effectors regulated by G proteins and their impact on cardiac function. G protein–independent signaling is a relatively newer concept that is being explored more frequently in the cardiovascular system. Recent studies have begun to reveal how cardiac function may be regulated via G protein–independent signaling, especially with respect to the ever-expanding cohort of β-arrestin–mediated processes. This review primarily focuses on the impact of both G protein–dependent and β-arrestin–dependent signaling pathways on cardiac function, highlighting the most recent data that illustrate the comprehensive nature of these mechanisms of G protein-coupled receptor signaling.