Evidence map›Paper›PMID 35878706›Full record

ReviewJournal of molecular and cellular cardiology2022

GRK2 in cardiovascular disease and its potential as a therapeutic target.

Kimberly M Ferrero, Walter J Koch

Abstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. GRK2 activates TRAF2-NF-Acta pharmaceutica Sinica. B · 2025
    Article
  6. Article
  7. Logic-based machine learning predicts how escitalopram attenuates cardiomyocyte hypertrophy.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. GRK2 and Mitochondrial Dynamics in Cardiovascular Health and Disease.International journal of molecular sciences · 2025
    Review
  9. Review
  10. Review
  11. Review
  12. The roles of G protein-coupled receptor kinase 2 in renal diseases.Journal of cellular and molecular medicine · 2024
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
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.

Kimberly M FerreroLewis Katz School of Medicine at Temple University, Department of Cardiovascular Sciences, Philadelphia, PA, USA; Lewis Katz School of Medicine at Temple University, Center for Translational Medicine, Philadelphia, PA, USA.
Walter J KochLewis Katz School of Medicine at Temple University, Department of Cardiovascular Sciences, Philadelphia, PA, USA; Lewis Katz School of Medicine at Temple University, Center for Translational Medicine, Philadelphia, PA, USA. Electronic address: walter.koch@temple.edu.
Temple University · US

Funding

Regulation of Beta-Adrenergic Receptor Signaling by S-NitrosylationP01HL075443 · NHLBI · DUKE UNIVERSITY · PI ROCKMAN, HOWARD A · 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
Small and large animal surgery, physiology and histologyP01HL134608 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI Walter J. Koch · 2017 to 2026
$21.0M
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
Integrative Cardiovascular PathophysiologyT32HL091804 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI ELROD, JOHN WILLIAM · 2008 to 2024
$4.5M
Targeting GRK2 in the HeartR01HL061690 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI KOCH, WALTER J. · 1998 to 2022
$4.2M
Role of S-Nitrosylation on Beta-Adrenergic Signaling in Cardiac Injury and RepairR01HL157151 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI KOCH, WALTER J., STAMLER, JONATHAN S. · 2021 to 2024
$2.8M
Novel roles for mtGRK2 in heart failure pathogenesisF31HL154567 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI FERRERO, KIMBERLY · 2021 to 2022
$37k
American Heart Association-American Stroke Association 18MERIT33900036NHLBI NIH HHS F31 HL154567NHLBI NIH HHS P01 HL075443NHLBI NIH HHS P01 HL091799NHLBI NIH HHS P01 HL108806NHLBI NIH HHS P01 HL134608NHLBI NIH HHS R01 HL061690NHLBI NIH HHS R01 HL071818NHLBI NIH HHS R01 HL157151NHLBI NIH HHS T32 HL091804
6 · The paper itself

Abstract

Cardiovascular diseases (CVDs) represent the leading cause of death globally. Despite major advances in the field of pharmacological CVD treatments, particularly in the field of heart failure (HF) research, case numbers and overall mortality remain high and have trended upwards over the last few years. Thus, identifying novel molecular targets for developing HF therapeutics remains a key research focus. G protein-coupled receptors (GPCRs) are critical myocardial signal transducers which regulate cardiac contractility, growth, adaptation and metabolism. Additionally, GPCR dysregulation underlies multiple models of cardiac pathology, and most pharmacological therapeutics currently used in HF target these receptors. Currently-approved treatments have improved patient outcomes, but therapies to stop or reverse HF are lacking. A recent focus on GPCR intracellular-regulating proteins such as GPCR kinases (GRKs) has uncovered GRK2 as a promising target for combating HF. Current literature strongly establishes increased levels and activity of GRK2 in multiple models of CVD. Additionally, the GRK2 interactome includes numerous proteins which interact with differential domains of GRK2 to modulate both beneficial and deleterious signaling pathways in the heart, indicating that these domains can be targeted with a high level of specificity unique to various cardiac pathologies. These data support the premise that GRK2 should be at the forefront of a novel investigative drug search. This perspective reviews cardiac GPCRs, describes the structure and functions of GRK2 in cardiac function and maladaptive pathology, and summarizes the ongoing and future research for targeting this critical kinase across cellular, animal and human models of cardiac dysfunction and HF.

Indexed as

Cardiovascular DiseasesG-Protein-Coupled Receptor Kinase 2Heart FailureAnimalsHumansMyocardiumReceptors, G-Protein-CoupledG-Protein-Coupled Receptor Kinase 2GRK2 protein, humanReceptors, G-Protein-CoupledCardiovascular diseaseGPCRGRK2Heart failureParoxetine

Identifiers

PMID35878706
PMCPMC12186197
OpenAlexW4286636749

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.