Evidence map›Paper›PMID 25834229›Full record

ReviewPhysiological reviews2015

The evolving impact of g protein-coupled receptor kinases in cardiac health and disease.

Priscila Y Sato, J Kurt Chuprun, Mathew Schwartz, Walter J Koch

Open access · greenAbstract readReview
In one paragraph

Review in Physiological reviews, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed, 1 pooled it
8.4field-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

101 citing papers in PubMed, 1 synthesis or guideline pooled it, 144 citations in OpenAlex.

  1. Pooled it
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  20. GRK2 in cardiovascular disease and its potential as a therapeutic target.Journal of molecular and cellular cardiology · 2022
    Review

41 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

4 authors at 2 institutions in 2 countries.

Priscila Y SatoCenter for Translational Medicine and Department of Pharmacology, Temple University School of Medicine, Philadelphia, Pennsylvania; and Advanced Institutes of Convergence Technology, Suwon, South Korea.
J Kurt ChuprunCenter for Translational Medicine and Department of Pharmacology, Temple University School of Medicine, Philadelphia, Pennsylvania; and Advanced Institutes of Convergence Technology, Suwon, South Korea.
Mathew SchwartzCenter for Translational Medicine and Department of Pharmacology, Temple University School of Medicine, Philadelphia, Pennsylvania; and Advanced Institutes of Convergence Technology, Suwon, South Korea.
Walter J KochCenter for Translational Medicine and Department of Pharmacology, Temple University School of Medicine, Philadelphia, Pennsylvania; and Advanced Institutes of Convergence Technology, Suwon, South Korea.
Advanced Institute of Convergence Technology · KRTemple University · US

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 HL091799NHLBI NIH HHS P01HL108806NHLBI NIH HHS P01 HL75443NHLBI NIH HHS R01 HL061690NHLBI NIH HHS R01 HL085503NHLBI NIH HHS R37 HL061690
6 · The paper itself

Abstract

G protein-coupled receptors (GPCRs) are important regulators of various cellular functions via activation of intracellular signaling events. Active GPCR signaling is shut down by GPCR kinases (GRKs) and subsequent β-arrestin-mediated mechanisms including phosphorylation, internalization, and either receptor degradation or resensitization. The seven-member GRK family varies in their structural composition, cellular localization, function, and mechanism of action (see sect. II). Here, we focus our attention on GRKs in particular canonical and novel roles of the GRKs found in the cardiovascular system (see sects. III and IV). Paramount to overall cardiac function is GPCR-mediated signaling provided by the adrenergic system. Overstimulation of the adrenergic system has been highly implicated in various etiologies of cardiovascular disease including hypertension and heart failure. GRKs acting downstream of heightened adrenergic signaling appear to be key players in cardiac homeostasis and disease progression, and herein we review the current data on GRKs related to cardiac disease and discuss their potential in the development of novel therapeutic strategies in cardiac diseases including heart failure.

Indexed as

Signal TransductionAnimalsG-Protein-Coupled Receptor Kinase 2G-Protein-Coupled Receptor Kinase 5G-Protein-Coupled Receptor KinasesHeart DiseasesHumansMyocardiumReceptors, G-Protein-CoupledG-Protein-Coupled Receptor Kinase 2G-Protein-Coupled Receptor Kinase 5G-Protein-Coupled Receptor KinasesReceptors, G-Protein-Coupled

Identifiers

PMID25834229
PMCPMC4551214
OpenAlexW2335583226

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.