Evidence map›Paper›PMID 29320510›Full record

ArticlePLoS genetics2018

Adipose tissue ATGL modifies the cardiac lipidome in pressure-overload-induced left ventricular failure.

Janek Salatzki, Anna Foryst-Ludwig, Kajetan Bentele, Annelie Blumrich, Elia Smeir, Zsofia Ban, Sarah Brix, Jana Grune, Niklas Beyhoff, Robert Klopfleisch and 11 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 60 citations in OpenAlex.

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  12. Vascular ATGL-dependent lipolysis and the activation of cPLACellular and molecular life sciences : CMLS · 2024
    Article
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  19. Transcriptome and metabolome changes induced by bitter melon (Journal of traditional and complementary medicine · 2022
    Article
  20. Small-Molecule Inhibitors Targeting Lipolysis in Human Adipocytes.Journal of the American Chemical Society · 2022
    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

21 authors at 9 institutions in 2 countries.

Janek SalatzkiCharité-Universitaetsmedizin, Institute of Pharmacology, Center for Cardiovascular Research, Berlin, Germany.
Anna Foryst-LudwigCharité-Universitaetsmedizin, Institute of Pharmacology, Center for Cardiovascular Research, Berlin, Germany.
Kajetan BenteleBerlin Institute of Health, BIH, Core Unit Bioinformatics, Berlin, Germany.
Annelie BlumrichCharité-Universitaetsmedizin, Institute of Pharmacology, Center for Cardiovascular Research, Berlin, Germany.
Elia SmeirCharité-Universitaetsmedizin, Institute of Pharmacology, Center for Cardiovascular Research, Berlin, Germany.
Zsofia BanCharité-Universitaetsmedizin, Institute of Pharmacology, Center for Cardiovascular Research, Berlin, Germany.
Sarah BrixCharité-Universitaetsmedizin, Institute of Pharmacology, Center for Cardiovascular Research, Berlin, Germany.
Jana GruneCharité-Universitaetsmedizin, Institute of Pharmacology, Center for Cardiovascular Research, Berlin, Germany.
Niklas BeyhoffCharité-Universitaetsmedizin, Institute of Pharmacology, Center for Cardiovascular Research, Berlin, Germany.
Robert KlopfleischDepartment of Veterinary Pathology, Freie Universität Berlin, Berlin, Germany.
Sebastian DunstDepartment of Experimental Toxicology and ZEBET, German Centre for the Protection of Laboratory Animals (Bf3R), German Federal Institute for Risk Assessment, Berlin, Germany.
Michal A SurmaLipotype GmbH, Dresden, Germany.ORCID 0000-0001-7833-2214
Christian KloseLipotype GmbH, Dresden, Germany.
Michael RotheLipidomix GmbH, Berlin, Germany.
Frank R HeinzelDZHK (German Centre for Cardiovascular Research), partner site Berlin, Germany.
Alexander KrannichCoordination Center for Clinical Trials, Charité-Universitaetsmedizin/ BIH, Berlin, Germany.ORCID 0000-0002-4025-6495
Erin E KershawDivision of Endocrinology and Metabolism, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.ORCID 0000-0002-3887-4868
Dieter BeuleBerlin Institute of Health, BIH, Core Unit Bioinformatics, Berlin, Germany.
P Christian SchulzeDepartment of Internal Medicine I, Division of Cardiology, Angiology, Pneumology and Intensive Medical Care, University Hospital Jena, Friedrich-Schiller-University Jena, Germany.
Nikolaus MarxDepartment of Internal Medicine I, Cardiology, Angiology, Pneumology and Internal Intensive Care Medicine, University Hospital, RWTH Aachen, Aachen, Germany.
Ulrich KintscherCharité-Universitaetsmedizin, Institute of Pharmacology, Center for Cardiovascular Research, Berlin, Germany.ORCID 0000-0001-7386-0990
German Centre for Cardiovascular Research · DECharité - Universitätsmedizin Berlin · DEMax Delbrück Center · DEFederal Institute for Risk Assessment · DEFreie Universität Berlin · DEFriedrich Schiller University Jena · DELipidomix (Germany) · DERWTH Aachen University · DEUniversity of Pittsburgh · US

Funding

Cardiac Lipotoxicity and Ceramide Metabolism in Heart FailureR01HL114813 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI COLOMBO, PAOLO C, SCHULZE, P. CHRISTIAN · 2013 to 2017
$3.0M
Adipose Triglyceride Lipase (ATGL) in Lipotoxicity and The Metabolic SyndromeR01DK090166 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KERSHAW, ERIN E. · 2011 to 2015
$1.7M
NHLBI NIH HHS R01 HL114813NIDDK NIH HHS R01 DK090166
6 · The paper itself

Abstract

Adipose tissue lipolysis occurs during the development of heart failure as a consequence of chronic adrenergic stimulation. However, the impact of enhanced adipose triacylglycerol hydrolysis mediated by adipose triglyceride lipase (ATGL) on cardiac function is unclear. To investigate the role of adipose tissue lipolysis during heart failure, we generated mice with tissue-specific deletion of ATGL (atATGL-KO). atATGL-KO mice were subjected to transverse aortic constriction (TAC) to induce pressure-mediated cardiac failure. The cardiac mouse lipidome and the human plasma lipidome from healthy controls (n = 10) and patients with systolic heart failure (HFrEF, n = 13) were analyzed by MS-based shotgun lipidomics. TAC-induced increases in left ventricular mass (LVM) and diastolic LV inner diameter were significantly attenuated in atATGL-KO mice compared to wild type (wt) -mice. More importantly, atATGL-KO mice were protected against TAC-induced systolic LV failure. Perturbation of lipolysis in the adipose tissue of atATGL-KO mice resulted in the prevention of the major cardiac lipidome changes observed after TAC in wt-mice. Profound changes occurred in the lipid class of phosphatidylethanolamines (PE) in which multiple PE-species were markedly induced in failing wt-hearts, which was attenuated in atATGL-KO hearts. Moreover, selected heart failure-induced PE species in mouse hearts were also induced in plasma samples from patients with chronic heart failure. TAC-induced cardiac PE induction resulted in decreased PC/ PE-species ratios associated with increased apoptotic marker expression in failing wt-hearts, a process absent in atATGL-KO hearts. Perturbation of adipose tissue lipolysis by ATGL-deficiency ameliorated pressure-induced heart failure and the potentially deleterious cardiac lipidome changes that accompany this pathological process, namely the induction of specific PE species. Non-cardiac ATGL-mediated modulation of the cardiac lipidome may play an important role in the pathogenesis of chronic heart failure.

Indexed as

AcyltransferasesAdipose TissueAnimalsCase-Control StudiesCells, CulturedHeart FailureHumansHypertensionLipaseLipid MetabolismMaleMetabolomeMiceMice, KnockoutMyocardiumMyocytes, CardiacAcyltransferasesLipasePNPLA2 protein, mouse

Identifiers

PMID29320510
PMCPMC5779697
OpenAlexW2782945295

What OpenQuestion holds

Textmetadata
LicenceCC BY
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Registered trials

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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.