Evidence map›Paper›PMID 32429302›Full record

ArticleCells2020

CTRP9 Mediates Protective Effects in Cardiomyocytes via AMPK- and Adiponectin Receptor-Mediated Induction of Anti-Oxidant Response.

Bernd Niemann, Ling Li, Dorothee Siegler, Benedikt H Siegler, Fabienne Knapp, Jakob Hanna, Muhammad Aslam, Michael Kracht, Rainer Schulz, Susanne Rohrbach

Open access · goldAbstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 28 citations in OpenAlex.

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  9. AMPK and the Challenge of Treating Hypoxic Pulmonary Hypertension.International journal of molecular sciences · 2022
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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

10 authors at 1 institution in 1 country.

Bernd NiemannDepartment of Cardiac and Vascular Surgery, Justus Liebig University Giessen, 35392 Giessen, Germany.
Ling LiInstitute of Physiology, Justus Liebig University Giessen, 35392 Giessen, Germany.
Dorothee SieglerInstitute of Physiology, Justus Liebig University Giessen, 35392 Giessen, Germany.
Benedikt H SieglerInstitute of Physiology, Justus Liebig University Giessen, 35392 Giessen, Germany.
Fabienne KnappInstitute of Physiology, Justus Liebig University Giessen, 35392 Giessen, Germany.
Jakob HannaInstitute of Physiology, Justus Liebig University Giessen, 35392 Giessen, Germany.
Muhammad AslamDepartment of Cardiology and Angiology, Justus Liebig University Giessen, 35392 Giessen, Germany.ORCID 0000-0002-8529-4217
Michael KrachtRudolf Buchheim Institute of Pharmacology, Justus Liebig University Giessen, 35392 Giessen, Germany.ORCID 0000-0002-8501-043X
Rainer SchulzInstitute of Physiology, Justus Liebig University Giessen, 35392 Giessen, Germany.
Susanne RohrbachInstitute of Physiology, Justus Liebig University Giessen, 35392 Giessen, Germany.
Justus-Liebig-Universität Gießen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The C1q/tumor necrosis factor-alpha-related protein 9 (CTRP9) has been reported to exert cardioprotective effects, but its role in the right ventricle (RV) remains unclear. To investigate the role of CTRP9 in RV hypertrophy and failure, we performed pulmonary artery banding in weanling rats to induce compensatory RV hypertrophy seven weeks after surgery and RV failure 22 weeks after surgery. CTRP9 expression, signal transduction and mechanisms involved in protective CTRP9 effects were analyzed in rat and human RV tissue and cardiac cells. We demonstrate that CTRP9 was induced during compensatory RV hypertrophy but almost lost at the stage of RV failure. RV but not left ventricular (LV) cardiomyocytes or RV endothelial cells demonstrated increased intracellular reactive oxygen species (ROS) and apoptosis activation at this stage. Exogenous CTRP9 induced AMP-activated protein kinase (AMPK)-dependent transcriptional activation of the anti-oxidant thioredoxin-1 (Trx1) and superoxide dismutase-2 (SOD2) and reduced phenylephrine-induced ROS. Combined knockdown of adiponectin receptor-1 (AdipoR1) and AdipoR2 or knockdown of calreticulin attenuated CTRP9-mediated anti-oxidant effects. Immunoprecipitation showed an interaction of AdipoR1 with AdipoR2 and the co-receptor T-cadherin, but no direct interaction with calreticulin. Thus, CTRP9 mediates cardioprotective effects through inhibition of ROS production induced by pro-hypertrophic agents via AMPK-mediated activation of anti-oxidant enzymes.

Indexed as

AdiponectinAMP-Activated Protein KinasesAnimalsAnimals, NewbornAntioxidantsCardiotonic AgentsDisease Models, AnimalGene Expression RegulationGlycoproteinsHeart VentriclesHEK293 CellsHumansHuman Umbilical Vein Endothelial CellsMaleModels, BiologicalMyocytes, CardiacAdiponectinAMP-Activated Protein KinasesAntioxidantsC1QTNF9B protein, humanC1qtnf9 protein, ratCardiotonic AgentsCTRP9 protein, mouseGlycoproteinsReactive Oxygen SpeciesReceptors, AdiponectinAMPKC1q familycardiomyocyteheart failureROS

Identifiers

PMID32429302
PMCPMC7291146
OpenAlexW3025945819

What OpenQuestion holds

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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.