title: 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.
authors: Department of Pharmaceutical Sciences, Jefferson School of Pharmacy, and Center for Translational Medicine, Thomas Jefferson University, 1025 Walnut Street, 402 College Building, Philadelphia, PA 19107, USA. douglas.tilley@jefferson.edu
authors: Douglas G
authors: DG
authors: Tilley
mesh_terms: D019390:Arrestins / Q000378:metabolism; D006321:Heart / Q000502:physiology*; D006801:Humans; D043562:Receptors, G-Protein-Coupled / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology*; D000071557:beta-Arrestins
chemical_list: D019390:Arrestins; D043562:Receptors, G-Protein-Coupled; D000071557:beta-Arrestins