Evidence map›Paper›PMID 21622221›Full record

ReviewFrontiers in bioscience (Landmark edition)2011

G protein-coupled receptor kinases in normal and failing myocardium.

Zheng Maggie Huang, Jessica I Gold, Walter J Koch

Open access · bronzeAbstract readReview
In one paragraph

Review in Frontiers in bioscience (Landmark edition), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

47 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Differential Regulation of GPCRs-Are GRK Expression Levels the Key?Frontiers in cell and developmental biology · 2021
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Prolonged ATScientific reports · 2017
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Dual role of GRK5 in cancer development and progression.Translational medicine @ UniSa · 2016
    Article
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.

Zheng Maggie HuangCenter for Translational Medicine and George Zallie and Family Laboratory for Cardiovascular Gene Therapy, Department of Medicine, Thomas Jefferson University, Philadelphia, PA, USA.
Jessica I Gold
Walter J Koch
Thomas Jefferson 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
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 R01 HL061690NHLBI NIH HHS R01 HL085503NHLBI NIH HHS R01 HL58803NHLBI NIH HHS R37 HL061690PHS HHS P01 091799
6 · The paper itself

Abstract

Heart failure (HF) is the end stage of many underlying cardiovascular diseases and is among the leading causes of morbidity and mortality in industrialized countries. One of the striking characteristics of HF is the desensitization of G protein-coupled receptor (GPCR) signaling, particularly the beta-adrenergic receptor (betaAR) system. GPCR desensitization is initiated by phosphorylation by GPCR kinases (GRKs), followed by downregulation and functional uncoupling from their G proteins. In the heart, the major GRK isoforms, GRK2 and GRK5, undergo upregulation due to the heightened sympathetic nervous system activity that is characteristic of HF as catecholamine levels increase in an effort to drive the failing pump. This desensitization leads to the distinctive loss of inotropic reserve and functional capacity of the failing heart. Moreover, GRK2 and GRK5 have an increasing non-GPCR interactome, which may play critical roles in cardiac physiology. In the current review, the canonical GPCR kinase function of GRKs and the novel non-GPCR kinase activity of GRKs, their contribution to the pathogenesis of cardiac hypertrophy and HF, and the possibility of GRKs serving as future drug targets will be discussed.

Indexed as

AnimalsGenetic TherapyG-Protein-Coupled Receptor Kinase 2G-Protein-Coupled Receptor Kinase 5G-Protein-Coupled Receptor KinasesHeart FailureHumansMiceMice, TransgenicModels, CardiovascularMyocardiumPolymorphism, Single NucleotideProtein Structure, TertiaryReceptors, Adrenergic, betaReceptors, G-Protein-CoupledSignal TransductionG-Protein-Coupled Receptor Kinase 2G-Protein-Coupled Receptor Kinase 5G-Protein-Coupled Receptor KinasesReceptors, Adrenergic, betaReceptors, G-Protein-Coupled

Identifiers

PMID21622221
PMCPMC4149910
OpenAlexW2027565281

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.