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.