Evidence map›Paper›PMID 28077324›Full record

ReviewCellular signalling2018

GRK2 as negative modulator of NO bioavailability: Implications for cardiovascular disease.

Alessandro Cannavo, Walter J Koch

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cellular signalling, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Endocan as a marker of endothelial dysfunction in hypertension: a systematic review and meta-analysis.Hypertension research : official journal of the Japanese Society of Hypertension · 2023
    Pooled it
  2. Review
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  4. Article
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  10. β-Arrestin2 is a critical component of the GPCR-eNOS signalosome.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
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  12. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Alessandro CannavoCenter for Translational Medicine and Department of Pharmacology, Lewis Katz School of Medicine, Temple University, Philadelphia, USA.
Walter J KochCenter for Translational Medicine and Department of Pharmacology, Lewis Katz School of Medicine, Temple University, Philadelphia, USA. Electronic address: walter.koch@temple.edu.
Temple University · US

Funding

Regulation of Beta-Adrenergic Receptor Signaling by S-NitrosylationP01HL075443 · NHLBI · DUKE UNIVERSITY · PI XIAO, KUNHONG · 2004 to 2019
$26.1M
Targeted Cancer Therapeutics and Heart Failure: Mechanisms and Post-injury RepairP01HL091799 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI KOCH, WALTER J. · 2008 to 2018
$23.1M
PKC alpha as a translational target in Heart FailureP01HL108806 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI RABINOWITZ, JOSEPH E · 2012 to 2016
$11.3M
Structure, function, and inhibition of G protein-coupled receptor kinasesR01HL071818 · NHLBI · UNIVERSITY OF TEXAS AUSTIN · PI TESMER, JOHN · 2004 to 2023
$7.1M
Targeting GRK2 (BARK1) in Heart FailureR37HL061690 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI KOCH, WALTER J. · 2009 to 2018
$3.9M
NHLBI NIH HHS P01 HL075443NHLBI NIH HHS P01 HL091799NHLBI NIH HHS P01 HL108806NHLBI NIH HHS R01 HL071818NHLBI NIH HHS R37 HL061690
6 · The paper itself

Abstract

Nitric oxide (NO), initially identified as endothelium-derived relaxing factor (EDRF), is a gaso-transmitter with important regulatory roles in the cardiovascular, nervous and immune systems. In the former, this diatomic molecule and free radical gas controls vascular tone and cardiac mechanics, among others. In the cardiovascular system, it is now understood that β-adrenergic receptor (βAR) activation is a key modulator of NO generation. Therefore, it is not surprising that the up-regulation of G protein-coupled receptor kinases (GRKs), in particular GRK2, that restrains βAR activity contributes to impaired cardiovascular functions via alteration of NO bioavailability. This review, will explore the specific interrelation between βARs, GRK2 and NO in the cardiovascular system and their inter-relationship for the pathogenesis of the onset of disease. Last, we will update the readers on the current status of GRK2 inhibitors as a potential therapeutic strategy for heart failure with an emphasis on their ability of rescuing NO bioavailability.

Indexed as

AnimalsCardiovascular DiseasesG-Protein-Coupled Receptor Kinase 2HumansModels, AnimalNitric OxideProtein Kinase InhibitorsReceptors, Adrenergic, betaUp-RegulationG-Protein-Coupled Receptor Kinase 2Nitric OxideProtein Kinase InhibitorsReceptors, Adrenergic, betaCardiovascular systemG protein-coupled receptor kinaseNitric oxideβ-adrenergic receptor

Identifiers

PMID28077324
PMCPMC5500446
OpenAlexW2570328057

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.