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G-Protein-Coupled Receptors and Their Kinases in Cardiac Regulation

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G Protein-Coupled Receptor Kinases

Part of the book series: Methods in Pharmacology and Toxicology ((MIPT))

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Abstract

The superfamily of G-protein-coupled receptors (GPCRs), or seven transmembrane-spanning receptors (7TMRs), represents the largest family of membrane proteins that transduce cell signals via heterotrimeric G proteins from neurohormones, ions, and sensory stimuli to regulate virtually every aspect of mammalian physiology. In the normal and diseased heart, it is apparent that major players include the β-adrenergic receptors (βARs) and the angiotensin II type 1 receptors (AT1Rs). Their crucial role is reflected by the fact that, currently, they represent the direct targets of different approved cardiovascular drugs used in clinical practice. However, other “minor” receptors and their signaling pathways have been identified for roles that they exert on cardiac pathophysiology. GPCRs can, individually or collectively, regulate cardiac growth and function, including processes such as heart rate, contractility, and blood pressure, in response to catecholamines and other neurohormones. For these reasons, GPCRs are dynamically regulated to prevent overstimulation that could lead to cardiac diseases like heart failure (HF). This dampening process, known as desensitization, is initiated through GPCR phosphorylation by second-messenger kinases like protein kinase A (PKA) and PKC or the GPCR kinases (GRKs). PKA and PKC initiate heterologous desensitization, while GRKs initiate homologous desensitization, phosphorylating only agonist-occupied GPCRs. This GPCR regulation by GRKs induces recruitment and binding of β-arrestins that displace bound G proteins, therefore uncoupling receptors from their downstream signaling effectors. This process continues through β-arrestin-dependent internalization of receptors, that lead either to their degradation and downregulation or recycling (resensitization) to the membrane. Moreover, β-arrestin recruitment to GRK-phosphorylated receptors has been shown to lead to intracellular signaling, a process called G protein-dependent and independent signaling. Given their central role in cardiac physiology and in pathology, GPCRs are critical therapeutic targets in cardiac diseases and GRKs are emerging as innovative targets.

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Authors and Affiliations

  1. Department of Pharmacology, Center for Translational Medicine, School of Medicine, Temple University, 3500 N. Broad Street, MERB 941, Philadelphia, PA, 19140, USA

    Alessandro Cannavo, Claudio de Lucia & Walter J. Koch Ph.D., F.A.H.A.

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  1. Alessandro Cannavo
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  2. Claudio de Lucia
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  3. Walter J. Koch Ph.D., F.A.H.A.
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Correspondence to Walter J. Koch Ph.D., F.A.H.A. .

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Editors and Affiliations

  1. Department of Pharmacology, Vanderbilt University , NASHVILLE, Tennessee, USA

    Vsevolod V. Gurevich

  2. Department of Pharmacology, Vanderbilt University, Nashville, Tennessee, USA

    Eugenia V. Gurevich

  3. Life Sciences Institute, University of Michigan, Ann Arbor, Michigan, USA

    John J.G. Tesmer

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Cannavo, A., de Lucia, C., Koch, W.J. (2016). G-Protein-Coupled Receptors and Their Kinases in Cardiac Regulation. In: Gurevich, V., Gurevich, E., Tesmer, J. (eds) G Protein-Coupled Receptor Kinases. Methods in Pharmacology and Toxicology. Humana Press, New York, NY. https://doi.org/10.1007/978-1-4939-3798-1_12

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