Evidence map›Paper›PMID 27577581›Full record

ArticleJournal of the American Heart Association2016

Gut Microbiota Promote Angiotensin II-Induced Arterial Hypertension and Vascular Dysfunction.

Susanne H Karbach, Tanja Schönfelder, Ines Brandão, Eivor Wilms, Nives Hörmann, Sven Jäckel, Rebecca Schüler, Stefanie Finger, Maike Knorr, Jeremy Lagrange and 7 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 237 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
237citing papers in PubMed, 1 pooled it
13.4field-weighted citation impact, top 1% 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

237 citing papers in PubMed, 1 synthesis or guideline pooled it, 381 citations in OpenAlex.

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177 more citing papers are in PubMed but not listed here.

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 4 institutions in 1 country.

Susanne H KarbachCenter for Thrombosis and Hemostasis Mainz, Partner Site RheinMain, Mainz, Germany Center for Cardiology, Partner Site RheinMain, Mainz, Germany.
Tanja SchönfelderCenter for Thrombosis and Hemostasis Mainz, Partner Site RheinMain, Mainz, Germany.
Ines BrandãoCenter for Thrombosis and Hemostasis Mainz, Partner Site RheinMain, Mainz, Germany.
Eivor WilmsCenter for Thrombosis and Hemostasis Mainz, Partner Site RheinMain, Mainz, Germany.
Nives HörmannCenter for Thrombosis and Hemostasis Mainz, Partner Site RheinMain, Mainz, Germany.
Sven JäckelCenter for Thrombosis and Hemostasis Mainz, Partner Site RheinMain, Mainz, Germany.
Rebecca SchülerCenter for Thrombosis and Hemostasis Mainz, Partner Site RheinMain, Mainz, Germany Institute of Molecular Medicine, University Medical Center Mainz, Mainz, Germany.
Stefanie FingerCenter for Thrombosis and Hemostasis Mainz, Partner Site RheinMain, Mainz, Germany.
Maike KnorrCenter for Thrombosis and Hemostasis Mainz, Partner Site RheinMain, Mainz, Germany Center for Cardiology, Partner Site RheinMain, Mainz, Germany.
Jeremy LagrangeCenter for Thrombosis and Hemostasis Mainz, Partner Site RheinMain, Mainz, Germany.
Moritz BrandtCenter for Thrombosis and Hemostasis Mainz, Partner Site RheinMain, Mainz, Germany Center for Cardiology, Partner Site RheinMain, Mainz, Germany.
Ari WaismanInstitute of Molecular Medicine, University Medical Center Mainz, Mainz, Germany.
Sabine KossmannCenter for Thrombosis and Hemostasis Mainz, Partner Site RheinMain, Mainz, Germany Center for Cardiology, Partner Site RheinMain, Mainz, Germany.
Katrin SchäferCenter for Thrombosis and Hemostasis Mainz, Partner Site RheinMain, Mainz, Germany Center for Cardiology, Partner Site RheinMain, Mainz, Germany.
Thomas MünzelCenter for Thrombosis and Hemostasis Mainz, Partner Site RheinMain, Mainz, Germany Center for Cardiology, Partner Site RheinMain, Mainz, Germany German Center for Cardiovascular Research (DZHK), Partner Site RheinMain, Mainz, Germany.
Christoph ReinhardtCenter for Thrombosis and Hemostasis Mainz, Partner Site RheinMain, Mainz, Germany German Center for Cardiovascular Research (DZHK), Partner Site RheinMain, Mainz, Germany.
Philip WenzelCenter for Thrombosis and Hemostasis Mainz, Partner Site RheinMain, Mainz, Germany Center for Cardiology, Partner Site RheinMain, Mainz, Germany German Center for Cardiovascular Research (DZHK), Partner Site RheinMain, Mainz, Germany wenzelp@uni-mainz.de.
RheinMain University of Applied Sciences · DEGerman Centre for Cardiovascular Research · DEJohannes Gutenberg University Mainz · DEUniversity Medical Center of the Johannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe gut microbiome is essential for physiological host responses and development of immune functions. The impact of gut microbiota on blood pressure and systemic vascular function, processes that are determined by immune cell function, is unknown. METHODS AND

resultsUnchallenged germ-free mice (GF) had a dampened systemic T helper cell type 1 skewing compared to conventionally raised (CONV-R) mice. Colonization of GF mice with regular gut microbiota induced lymphoid mRNA transcription of T-box expression in T cells and resulted in mild endothelial dysfunction. Compared to CONV-R mice, angiotensin II (AngII; 1 mg/kg per day for 7 days) infused GF mice showed reduced reactive oxygen species formation in the vasculature, attenuated vascular mRNA expression of monocyte chemoattractant protein 1 (MCP-1), inducible nitric oxide synthase (iNOS) and NADPH oxidase subunit Nox2, as well as a reduced upregulation of retinoic-acid receptor-related orphan receptor gamma t (Rorγt), the signature transcription factor for interleukin (IL)-17 synthesis. This resulted in an attenuated vascular leukocyte adhesion, less infiltration of Ly6G(+) neutrophils and Ly6C(+) monocytes into the aortic vessel wall, protection from kidney inflammation, as well as endothelial dysfunction and attenuation of blood pressure increase in response to AngII. Importantly, cardiac inflammation, fibrosis and systolic dysfunction were attenuated in GF mice, indicating systemic protection from cardiovascular inflammatory stress induced by AngII.

conclusionGut microbiota facilitate AngII-induced vascular dysfunction and hypertension, at least in part, by supporting an MCP-1/IL-17 driven vascular immune cell infiltration and inflammation.

Indexed as

Germ-Free LifeAngiotensin IIAnimalsAortaArterial PressureBlood VesselsCell AdhesionChemokine CCL2Endothelium, VascularGastrointestinal MicrobiomeHypertensionLeukocytesMiceMonocytesNADPH Oxidase 2Neutrophil InfiltrationAngiotensin IICcl2 protein, mouseChemokine CCL2Cybb protein, mouseNADPH Oxidase 2Nitric Oxide Synthase Type IINos2 protein, mouseNuclear Receptor Subfamily 1, Group F, Member 3Reactive Oxygen SpeciesRNA, Messengerangiotensin IIarterial hypertensiongut microbiotainflammationmonocytesvascular dysfunction

Identifiers

PMID27577581
PMCPMC5079031
OpenAlexW2508585495

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.