Evidence map›Paper›PMID 32251665›Full record

ArticleMolecular metabolism2020

Cross-omics analysis revealed gut microbiome-related metabolic pathways underlying atherosclerosis development after antibiotics treatment.

Ben Arpad Kappel, Lorenzo De Angelis, Michael Heiser, Marta Ballanti, Robert Stoehr, Claudia Goettsch, Maria Mavilio, Anna Artati, Omero A Paoluzi, Jerzy Adamski and 7 more

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 2 pooled it
3.8field-weighted citation impact, top 5% 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

53 citing papers in PubMed, 2 syntheses or guidelines pooled it, 82 citations in OpenAlex.

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  11. How the Microbiome Drives Cardiovascular Disease.The Surgical clinics of North America · 2025
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  13. Research progress in the role of gut microbiota in ethanol metabolism.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
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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

17 authors at 9 institutions in 6 countries.

Ben Arpad KappelDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy; Department of Internal Medicine 1, University Hospital Aachen, RWTH Aachen University, Aachen, Germany.
Lorenzo De AngelisDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy.
Michael HeiserMetabolomic discoveries GmbH, Potsdam, Germany; Metabolon Inc., Morrisville, NC, USA.
Marta BallantiDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy; Center for Atherosclerosis, Policlinico Tor Vergata, Rome, Italy.
Robert StoehrDepartment of Internal Medicine 1, University Hospital Aachen, RWTH Aachen University, Aachen, Germany.
Claudia GoettschDepartment of Internal Medicine 1, University Hospital Aachen, RWTH Aachen University, Aachen, Germany.
Maria MavilioDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy.
Anna ArtatiResearch Unit Molecular Endocrinology and Metabolism, Helmholtz Zentrum München, German Research Center for Environmental Health (GmbH), Neuherberg, Germany.
Omero A PaoluziGastroenterology Unit, Policlinico Tor Vergata, Rome, Italy.
Jerzy AdamskiResearch Unit Molecular Endocrinology and Metabolism, Helmholtz Zentrum München, German Research Center for Environmental Health (GmbH), Neuherberg, Germany; Lehrstuhl für Experimentelle Genetik, Technical University of Munich, Freising-Weihenstephan, Germany; German Center for Diabetes Research (DZD e.V.), Neuherberg, Germany; Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Geltrude MingroneDepartment of Internal Medicine, Catholic University, Rome, Italy; Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy; Diabetes and Nutritional Sciences, Hodgkin Building, Guy's Campus, King's College London, London, United Kingdom.
Bart StaelsUniversité Lille, INSERM, Centre Hospitalier Universitaire de Lille, Institut Pasteur de Lille, U1011-European Genomic Institute for Diabetes, Lille, France.
Remy BurcelinInstitut des Maladies Métaboliques et Cardiovasculaires, INSERM U1048, Toulouse, France; Université Paul Sabatier, Toulouse, France.
Giovanni MonteleoneDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy; Gastroenterology Unit, Policlinico Tor Vergata, Rome, Italy.
Rossella MenghiniDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy.
Nikolaus MarxDepartment of Internal Medicine 1, University Hospital Aachen, RWTH Aachen University, Aachen, Germany.
Massimo FedericiDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy; Center for Atherosclerosis, Policlinico Tor Vergata, Rome, Italy. Electronic address: federicm@uniroma2.it.
University of Rome Tor Vergata · ITUniversitätsklinikum Aachen · DEHelmholtz Zentrum München · DEInserm · FRMetabolon (United States) · USNational University of Singapore · SGPoliclinico Tor Vergata · ITUniversità Cattolica del Sacro Cuore · ITUniversité Toulouse III - Paul Sabatier · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe metabolic influence of gut microbiota plays a pivotal role in the pathogenesis of cardiometabolic diseases. Antibiotics affect intestinal bacterial diversity, and long-term usage has been identified as an independent risk factor for atherosclerosis-driven events. The aim of this study was to explore the interaction between gut dysbiosis by antibiotics and metabolic pathways with the impact on atherosclerosis development.

methodsWe combined oral antibiotics with different diets in an Apolipoprotein E-knockout mouse model linking gut microbiota to atherosclerotic lesion development via an integrative cross-omics approach including serum metabolomics and cecal 16S rRNA targeted metagenomic sequencing. We further investigated patients with carotid atherosclerosis compared to control subjects with comparable cardiovascular risk.

resultsHere, we show that increased atherosclerosis by antibiotics was connected to a loss of intestinal diversity and alterations of microbial metabolic functional capacity with a major impact on the host serum metabolome. Pathways that were modulated by antibiotics and connected to atherosclerosis included diminished tryptophan and disturbed lipid metabolism. These pathways were related to the reduction of certain members of Bacteroidetes and Clostridia by antibiotics in the gut. Patients with atherosclerosis presented a similar metabolic signature as those induced by antibiotics in our mouse model.

conclusionTaken together, this work provides insights into the complex interaction between intestinal microbiota and host metabolism. Our data highlight that detrimental effects of antibiotics on the gut flora are connected to a pro-atherogenic metabolic phenotype beyond classical risk factors.

Indexed as

AgedAnimalsAnti-Bacterial AgentsAtherosclerosisBacteriaCecumDisease ProgressionFecesFemaleGastrointestinal MicrobiomeHumansMaleMetabolic Networks and PathwaysMetabolomeMetabolomicsMiceAnti-Bacterial AgentsRNA, Ribosomal, 16SAntibioticsAtherosclerosisCross-omicsDysbiosisGut microbiotaMetabolic diversity

Identifiers

PMID32251665
PMCPMC7183232
OpenAlexW3011310155

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LicenceCC BY-NC-ND
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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.