Evidence map›Paper›PMID 28256297›Full record

ReviewTrends in endocrinology and metabolism: TEM2017

Insulin and β Adrenergic Receptor Signaling: Crosstalk in Heart.

Qin Fu, Qingtong Wang, Yang K Xiang

Abstract readReview
In one paragraph

Review in Trends in endocrinology and metabolism: TEM, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 43 citations in OpenAlex.

  1. Central βVeterinary research communications · 2026
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  13. Hyperinsulinemia blunts sympathetic vasoconstriction: a possible role of β-adrenergic activation.American journal of physiology. Regulatory, integrative and comparative physiology · 2021
    Article
  14. Article
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  16. Use of a Systematic Pharmacological Methodology to Explore the Mechanism of Shengmai Powder in Treating Diabetic Cardiomyopathy.Medical science monitor : international medical journal of experimental and clinical research · 2020
    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

3 authors at 3 institutions in 2 countries.

Qin FuDepartment of Pharmacology, School of Basic Medicine, Tongji Medical College, Hubei Key Laboratory of Drug Target Research and Pharmacodynamic Evaluation, Huazhong University of Science and Technology, Wuhan, China. Electronic address: fuqin@mails.tjmu.edu.cn.
Qingtong WangInstitute of Clinical Pharmacology, Key Laboratory of Anti-inflammatory and Immune Medicine, Ministry of Education, Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Anhui Medical University, Hefei, China. Electronic address: hfwqt727@163.com.
Yang K XiangDepartment of Pharmacology, University of California, Davis, CA, USA; VA Northern California Health Care System, Mather, CA, USA. Electronic address: ykxiang@ucdavis.edu.
Anhui Medical University · CNHuazhong University of Science and Technology · CNUniversity of California, Davis · US

Funding

Insulin Inhibition of beta-AR Signaling in the MyocardiumR01HL127764 · NHLBI · UNIVERSITY OF IOWA · PI ABEL, E DALE, XIANG, YANG K · 2015 to 2018
$2.4M
Cardiac Dysfunction in the Met Syndrome: Cross-talk between IR and bAR SignalingR01HL112413 · NHLBI · UNIVERSITY OF IOWA · PI ABEL, E DALE, XIANG, YANG K · 2015 to 2018
$1.6M
Insulin Resistance and Myocardial AutophagyR01HL108379 · NHLBI · UNIVERSITY OF UTAH · PI ABEL, E DALE · 2011 to 2014
$1.5M
NHLBI NIH HHS R01 HL108379NHLBI NIH HHS R01 HL112413NHLBI NIH HHS R01 HL127764
6 · The paper itself

Abstract

Recent advances show that insulin may affect β adrenergic receptor (βAR) signaling in the heart to modulate cardiac function in clinically relevant states, such as diabetes mellitus (DM) and heart failure (HF). Conversely, activation of βAR regulates cardiac glucose uptake and promotes insulin resistance (IR) in HF. Here, we discuss the recent characterization of the interaction between the cardiac insulin receptor (InsR) and βAR in the myocardium, in which insulin stimulation crosstalks with cardiac βAR via InsR substrate (IRS)-dependent and G-protein receptor kinase 2 (GRK2)-mediated phosphorylation of β

Indexed as

AnimalsCyclic Nucleotide Phosphodiesterases, Type 4HumansInsulinReceptors, Adrenergic, betaReceptors, Adrenergic, beta-2Signal TransductionCyclic Nucleotide Phosphodiesterases, Type 4InsulinReceptors, Adrenergic, betaReceptors, Adrenergic, beta-2

Identifiers

PMID28256297
PMCPMC5535765
OpenAlexW2594813031

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.