Evidence map›Paper›PMID 33919975›Full record

ArticleCells2021

Comparative Analysis of CTRP-Mediated Effects on Cardiomyocyte Glucose Metabolism: Cross Talk between AMPK and Akt Signaling Pathway.

Ling Li, Muhammad Aslam, Benedikt H Siegler, Bernd Niemann, Susanne Rohrbach

Open access · goldAbstract readComparative Study
In one paragraph

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Unraveling the Roles of HIF-1, HO-1, GLUT-1 and GLUT-4 in Myocardial Protection.International journal of drug discovery and pharmacology · 2024
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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

5 authors at 1 institution in 1 country.

Ling LiInstitute of Physiology, Justus Liebig University Giessen, 35392 Giessen, Germany.
Muhammad AslamExperimental Cardiology, Department of Cardiology and Angiology, Justus Liebig University Giessen, 35392 Giessen, Germany.ORCID 0000-0002-8529-4217
Benedikt H SieglerInstitute of Physiology, Justus Liebig University Giessen, 35392 Giessen, Germany.
Bernd NiemannDepartment of Cardiac and Vascular Surgery, Justus Liebig University Giessen, 35392 Giessen, Germany.
Susanne RohrbachInstitute of Physiology, Justus Liebig University Giessen, 35392 Giessen, Germany.ORCID 0000-0002-7523-5221
Justus-Liebig-Universität Gießen · DE

Funding

Deutsche Forschungsgemeinschaft Projektnummer 268555672 - SFB 1213, Project B03FCMH Flexifunds Mitochondrial Network consortium
6 · The paper itself

Abstract

C1q/tumor necrosis factor -alpha-related proteins (CTRPs) have been shown to mediate protective cardiovascular effects, but no data exists on their effects on glucose and fatty acid (FA) metabolism in cardiomyocytes. In the present study, adult rat cardiomyocytes and H9C2 cardiomyoblasts were stimulated with various recombinant CTRPs. Glucose or FA uptake, expression of genes involved in glucose or FA metabolism and the role of the AMP-activated protein kinase (AMPK) and Akt were investigated. Although most CTRPs induced an increase in phosphorylation of AMPK and Akt in cardiomyocytes, mainly CTRP2, 7, 9 and 13 induced GLUT1 and GLUT4 translocation and glucose uptake in cardiomyocytes, despite high structural similarities among CTRPs. AMPK inhibition reduced the CTRPs-mediated activation of Akt, while Akt inhibition did not impair AMPK activation. In addition, CTRP2, 7, 9 and 13 mediated strong effects on the expression of enzymes involved in glucose or FA metabolism. Loss of adiponectin receptor 1, which has been suggested to be involved in CTRP-induced signal transduction, abolished the effects of some but not all CTRPs on glucose metabolism. Targeting the AMPK signaling pathway via CTRPs may offer a therapeutic principle to restore glucose homeostasis by acting on glucose uptake independent of the Akt pathway.

Indexed as

Signal TransductionAgingAMP-Activated Protein KinasesAnimalsCell LineFatty AcidsGene Expression RegulationGlucoseGlucose Transporter Type 1MiceMyocytes, CardiacOrgan SpecificityPhosphorylationProteinsProto-Oncogene Proteins c-aktRatsAMP-Activated Protein KinasesFatty AcidsGlucoseGlucose Transporter Type 1ProteinsProto-Oncogene Proteins c-aktadiponectinAdipoRAktAMPKC1q familyglucose metabolism

Identifiers

PMID33919975
PMCPMC8070942
OpenAlexW3152538320

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.