Evidence map›Paper›PMID 31186538›Full record

ReviewNature reviews. Cardiology2019

G protein-coupled receptor kinases as therapeutic targets in the heart.

Jessica Pfleger, Kenneth Gresham, Walter J Koch

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cardiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 1 pooled it
7.3field-weighted citation impact, top 2% 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

81 citing papers in PubMed, 1 synthesis or guideline pooled it, 147 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. The Energetic Cost of Adrenergic Signaling in Primary Human Fibroblasts.bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. GRK2 activates TRAF2-NF-Acta pharmaceutica Sinica. B · 2025
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. A New GRK2 Inhibitor for Heart Failure.JACC. Basic to translational science · 2025
    Article
  17. Article
  18. Article
  19. Review
  20. Review

21 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Jessica PflegerCenter for Translational Medicine, Department of Pharmacology, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
Kenneth GreshamCenter for Translational Medicine, Department of Pharmacology, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
Walter J KochCenter for Translational Medicine, Department of Pharmacology, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA. walter.koch@temple.edu.ORCID http://orcid.org/0000-0002-8522-530X
Temple University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

G protein-coupled receptors (GPCRs) are critical cellular sensors that mediate numerous physiological processes. In the heart, multiple GPCRs are expressed on various cell types, where they coordinate to regulate cardiac function by modulating critical processes such as contractility and blood flow. Under pathological settings, these receptors undergo aberrant changes in expression levels, localization and capacity to couple to downstream signalling pathways. Conventional therapies for heart failure work by targeting GPCRs, such as β-adrenergic receptor and angiotensin II receptor antagonists. Although these treatments have improved patient survival, heart failure remains one of the leading causes of mortality worldwide. GPCR kinases (GRKs) are responsible for GPCR phosphorylation and, therefore, desensitization and downregulation of GPCRs. In this Review, we discuss the GPCR signalling pathways and the GRKs involved in the pathophysiology of heart disease. Given that increased expression and activity of GRK2 and GRK5 contribute to the loss of contractile reserve in the stressed and failing heart, inhibition of overactive GRKs has been proposed as a novel therapeutic approach to treat heart failure.

Indexed as

Adrenergic beta-AntagonistsAnimalsbeta-ArrestinsCatecholaminesCyclic AMP-Dependent Protein KinasesG-Protein-Coupled Receptor Kinase 2G-Protein-Coupled Receptor Kinase 5G-Protein-Coupled Receptor KinasesHeart DiseasesHeart FailureHumansMuscle ContractionMyocytes, CardiacPeptide FragmentsReceptors, AdrenergicRecombinant ProteinsAdrenergic beta-AntagonistsBARKct protein, recombinantbeta-ArrestinsCatecholaminesCyclic AMP-Dependent Protein KinasesG-Protein-Coupled Receptor Kinase 2G-Protein-Coupled Receptor Kinase 5G-Protein-Coupled Receptor KinasesGRK2 protein, humanGRK5 protein, humanPeptide FragmentsReceptors, AdrenergicRecombinant Proteins

Identifiers

PMID31186538
OpenAlexW2951096969

What OpenQuestion holds

Textmetadata
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.