Nitric Oxide and S-Nitrosylation in Cardiac Regulation: G Protein-Coupled Receptor Kinase-2 and β-Arrestins as Targets.

Tytuł:: Nitric Oxide and S-Nitrosylation in Cardiac Regulation: G Protein-Coupled Receptor Kinase-2 and β-Arrestins as Targets.
Autorzy:: Kayki-Mutlu G; Center for Translational Medicine, Temple University School of Medicine, Philadelphia, PA 19140, USA.; Faculty of Pharmacy, Department of Pharmacology, Ankara University, Tandogan, 06560 Ankara, Turkey.
Koch WJ; Center for Translational Medicine, Temple University School of Medicine, Philadelphia, PA 19140, USA.
Źródło:: International journal of molecular sciences [Int J Mol Sci] 2021 Jan 07; Vol. 22 (2). Date of Electronic Publication: 2021 Jan 07.
Typ publikacji:: Journal Article; Review
Język:: English
Imprint Name(s):: Original Publication: Basel, Switzerland : MDPI, [2000-
MeSH Terms:: G-Protein-Coupled Receptor Kinase 2/*genetics
Nitric Oxide/*genetics
Receptors, Adrenergic, beta/*genetics
beta-Arrestins/*genetics
Cyclic GMP/genetics ; Cyclic GMP-Dependent Protein Kinases/genetics ; Humans ; Nitric Oxide Synthase/genetics ; S-Nitrosothiols/metabolism ; Signal Transduction/genetics
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Grant Information:: P01 HL174841, P01 HL075443, P01 HL134608, P01 HL091799, R01 HL 061690 United States GF NIH HHS; 18MERIT33900036 AHA
Contributed Indexing:: Keywords: GRK2; S-nitrosylation; nitric oxide; β-arrestins
Substance Nomenclature:: 0 (Receptors, Adrenergic, beta)
0 (S-Nitrosothiols)
0 (beta-Arrestins)
31C4KY9ESH (Nitric Oxide)
EC 1.14.13.39 (Nitric Oxide Synthase)
EC 2.7.11.12 (Cyclic GMP-Dependent Protein Kinases)
EC 2.7.11.15 (GRK2 protein, human)
EC 2.7.11.16 (G-Protein-Coupled Receptor Kinase 2)
H2D2X058MU (Cyclic GMP)
Entry Date(s):: Date Created: 20210112 Date Completed: 20210330 Latest Revision: 20210330
Update Code:: 20240105
PubMed Central ID:: PMC7825736
DOI:: 10.3390/ijms22020521
PMID:: 33430208
: Czasopismo naukowe

Pełny tekst

Cardiac diseases including heart failure (HF), are the leading cause of morbidity and mortality globally. Among the prominent characteristics of HF is the loss of β-adrenoceptor (AR)-mediated inotropic reserve. This is primarily due to the derangements in myocardial regulatory signaling proteins, G protein-coupled receptor (GPCR) kinases (GRKs) and β-arrestins (β-Arr) that modulate β-AR signal termination via receptor desensitization and downregulation. GRK2 and β-Arr2 activities are elevated in the heart after injury/stress and participate in HF through receptor inactivation. These GPCR regulators are modulated profoundly by nitric oxide (NO) produced by NO synthase (NOS) enzymes through S-nitrosylation due to receptor-coupled NO generation. S-nitrosylation, which is NO-mediated modification of protein cysteine residues to generate an S-nitrosothiol (SNO), mediates many effects of NO independently from its canonical guanylyl cyclase/cGMP/protein kinase G signaling. Herein, we review the knowledge on the NO system in the heart and S-nitrosylation-dependent modifications of myocardial GPCR signaling components GRKs and β-Arrs.

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