Evidence map›Paper›PMID 24812353›Full record

ReviewCirculation research2014

G protein-coupled receptor kinase 2: a link between myocardial contractile function and cardiac metabolism.

Meryl C Woodall, Michele Ciccarelli, Benjamin P Woodall, Walter J Koch

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

46 citing papers in PubMed, 86 citations in OpenAlex.

  1. A New GRK2 Inhibitor for Heart Failure.JACC. Basic to translational science · 2025
    Article
  2. Review
  3. GRK2 in cardiovascular disease and its potential as a therapeutic target.Journal of molecular and cellular cardiology · 2022
    Review
  4. Review
  5. α1-Adrenergic receptor regulates papillary muscle and aortic segment contractile function via modulation of store-operated CaJournal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2021
    Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Hurdles to Cardioprotection in the Critically Ill.International journal of molecular sciences · 2019
    Review
  14. Review
  15. Review
  16. Article
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  18. 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

4 authors at 1 institution in 1 country.

Meryl C WoodallFrom the Department of Pharmacology, Center for Translational Medicine, Temple University, Philadelphia, PA (M.C.W., B.P.W., W.J.K.); and Department of Medicine and Surgery, University of Salerno, Salerno, Italy (M.C.).
Michele Ciccarelli
Benjamin P Woodall
Walter J Koch
University of Salerno · IT

Funding

Regulation of Beta-Adrenergic Receptor Signaling by S-NitrosylationP01HL075443 · NHLBI · DUKE UNIVERSITY · PI STAMLER, JONATHAN S. · 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
Targeting GRK2 in the HeartR01HL061690 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI KOCH, WALTER J. · 1998 to 2022
$4.2M
Targeting GRK2 (BARK1) in Heart FailureR37HL061690 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI KOCH, WALTER J. · 2009 to 2018
$3.9M
GRK and b-Arrestin Signaling in Cardiac RegenerationR01HL085503 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI KOCH, WALTER J. · 2007 to 2015
$3.0M
NHLBI NIH HHS P01 HL075443NHLBI NIH HHS P01 HL091799NHLBI NIH HHS P01 HL108806NHLBI NIH HHS R01 HL061690NHLBI NIH HHS R01 HL085503NHLBI NIH HHS R37 HL061690PHS HHS P01 HLHL091799
6 · The paper itself

Abstract

Heart failure (HF) causes a tremendous burden on the worldwide healthcare system, affecting >23 million people. There are many cardiovascular disorders that contribute to the development of HF and multiple risk factors that accelerate its occurrence, but regardless of its underlying cause, HF is characterized by a marked decrease in myocardial contractility and loss of pump function. One biomarker molecule consistently shown to be upregulated in human HF and several animal models is G protein-coupled receptor kinase-2 (GRK2), a kinase originally discovered to be involved in G protein-coupled receptor desensitization, especially β-adrenergic receptors. Higher levels of GRK2 can impair β-adrenergic receptor-mediated inotropic reserve and its inhibition, or molecular reduction has shown to improve pump function in several animal models including a preclinical pig model of HF. Recently, nonclassical roles for GRK2 in cardiovascular disease have been described, including negative regulation of insulin signaling, a role in myocyte cell survival and apoptotic signaling, and it has been shown to be localized in/on mitochondria. These new roles of GRK2 suggest that GRK2 may be a nodal link in the myocyte, influencing both cardiac contractile function and cell metabolism and survival and contributing to HF independent of its canonical role in G protein-coupled receptor desensitization. In this review, classical and nonclassical roles for GRK2 will be discussed, focusing on recently discovered roles for GRK2 in cardiomyocyte metabolism and the effects that these roles may have on myocardial contractile function and HF development.

Indexed as

AnimalsBiomarkersG-Protein-Coupled Receptor Kinase 2Heart FailureHumansMyocardial ContractionMyocytes, CardiacBiomarkersG-Protein-Coupled Receptor Kinase 2GRK2 protein, humanG-protein-coupled receptor kinase 2heart failuremetabolismmyocytes, cardiac

Identifiers

PMID24812353
PMCPMC4095756
OpenAlexW2527600172

What OpenQuestion 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 OpenQuestion graph.