Evidence map›Paper›PMID 31843471›Full record

ArticleVascular pharmacology

Microbiota are critical for vascular physiology: Germ-free status weakens contractility and induces sex-specific vascular remodeling in mice.

Jonnelle M Edwards, Shaunak Roy, Jeremy C Tomcho, Zachary J Schreckenberger, Saroj Chakraborty, Nicole R Bearss, Piu Saha, Cameron G McCarthy, Matam Vijay-Kumar, Bina Joe and 1 more

Abstract readComparative Study
In one paragraph

Article in Vascular pharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
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  7. Enterococcus faecalis: implications for host health.World journal of microbiology & biotechnology · 2024
    Review
  8. The gut microbiome as a modulator of arterial function and age-related arterial dysfunction.American journal of physiology. Heart and circulatory physiology · 2024
    Review
  9. Review
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  19. Ethanol: striking the cardiovascular system by harming the gut microbiota.American journal of physiology. Heart and circulatory physiology · 2021
    Review
  20. Review
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

11 authors at 1 institution in 1 country.

Jonnelle M EdwardsMicrobiome Consortium, Center for Hypertension and Precision Medicine, Department of Physiology and Pharmacology, University of Toledo College of Medicine & Life Sciences, Toledo, OH, USA.
Shaunak RoyMicrobiome Consortium, Center for Hypertension and Precision Medicine, Department of Physiology and Pharmacology, University of Toledo College of Medicine & Life Sciences, Toledo, OH, USA.
Jeremy C TomchoMicrobiome Consortium, Center for Hypertension and Precision Medicine, Department of Physiology and Pharmacology, University of Toledo College of Medicine & Life Sciences, Toledo, OH, USA.
Zachary J SchreckenbergerMicrobiome Consortium, Center for Hypertension and Precision Medicine, Department of Physiology and Pharmacology, University of Toledo College of Medicine & Life Sciences, Toledo, OH, USA.
Saroj ChakrabortyMicrobiome Consortium, Center for Hypertension and Precision Medicine, Department of Physiology and Pharmacology, University of Toledo College of Medicine & Life Sciences, Toledo, OH, USA.
Nicole R BearssMicrobiome Consortium, Center for Hypertension and Precision Medicine, Department of Physiology and Pharmacology, University of Toledo College of Medicine & Life Sciences, Toledo, OH, USA.
Piu SahaMicrobiome Consortium, Center for Hypertension and Precision Medicine, Department of Physiology and Pharmacology, University of Toledo College of Medicine & Life Sciences, Toledo, OH, USA.
Cameron G McCarthyMicrobiome Consortium, Center for Hypertension and Precision Medicine, Department of Physiology and Pharmacology, University of Toledo College of Medicine & Life Sciences, Toledo, OH, USA.
Matam Vijay-KumarMicrobiome Consortium, Center for Hypertension and Precision Medicine, Department of Physiology and Pharmacology, University of Toledo College of Medicine & Life Sciences, Toledo, OH, USA.
Bina JoeMicrobiome Consortium, Center for Hypertension and Precision Medicine, Department of Physiology and Pharmacology, University of Toledo College of Medicine & Life Sciences, Toledo, OH, USA.
Camilla F WenceslauMicrobiome Consortium, Center for Hypertension and Precision Medicine, Department of Physiology and Pharmacology, University of Toledo College of Medicine & Life Sciences, Toledo, OH, USA. Electronic address: Camilla.Wenceslau@utoledo.edu.
University of Toledo · US

Funding

Genetic, Epigenetic and Dietary Salt effects on Microbiota and HypertensionR01HL143082 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI JOE, BINA · 2018 to 2021
$2.6M
Formyl peptide receptor activation induces vascular plasticity and remodeling inhypertensionR01HL149762 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI WENCESLAU, CAMILLA FERREIRA · 2021 to 2025
$1.9M
Interplay between Dietary Fiber and Gut Microbiota in Hepatocellular CarcinomaR01CA219144 · NCI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI VIJAY-KUMAR, MATAM · 2017 to 2021
$1.6M
Intrarenal Arteries Sense N-formyl Peptides Leading to Vascular Injury in SepsisR00GM118885 · NIGMS · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI WENCESLAU, CAMILLA FERREIRA · 2019 to 2021
$746k
NCI NIH HHS R01 CA219144NHLBI NIH HHS R01 HL143082NHLBI NIH HHS R01 HL149762NIGMS NIH HHS R00 GM118885
6 · The paper itself

Abstract

Commensal microbiota within a holobiont contribute to the overall health of the host via mutualistic symbiosis. Disturbances in such symbiosis is prominently correlated with a variety of diseases affecting the modern society of humans including cardiovascular diseases, which are the number one contributors to human mortality. Given that a hallmark of all cardiovascular diseases is changes in vascular function, we hypothesized that depleting microbiota from a holobiont would induce vascular dysfunction. To test this hypothesis, young mice of both sexes raised in germ-free conditions were examined vascular contractility and structure. Here we observed that male and female germ-free mice presented a decrease in contraction of resistance arteries. These changes were more pronounced in germ-free males than in germ-free females mice. Furthermore, there was a distinct change in vascular remodeling between males and females germ-free mice. Resistance arteries from male germ-free mice demonstrated increased vascular stiffness, as shown by the leftward shift in the stress-strain curve and inward hypotrophic remodeling, a characteristic of chronic reduction in blood flow. On the other hand, resistance arteries from germ-free female mice were similar in the stress-strain curves to that of conventionally raised mice, but were distinctly different and showed outward hypertrophic remodeling, a characteristic seen in aging. Interestingly, we observed that reactive oxygen species (ROS) generation from bone marrow derived neutrophils is blunted in female germ-free mice, but it is exacerbated in male germ-free mice. In conclusion, these observations indicate that commensal microbiota of a holobiont are central to maintain proper vascular function and structure homeostasis, especially in males.

Indexed as

Vascular RemodelingVasoconstrictionAnimalsBacteriaElastic ModulusFemaleGastrointestinal MicrobiomeGerm-Free LifeHost Microbial InteractionsMaleMesenteric ArteriesMice, Inbred C57BLNeutrophilsReactive Oxygen SpeciesSex FactorsVascular ResistanceReactive Oxygen SpeciesGerm-free miceSex differencesVascular contractility

Identifiers

PMID31843471
PMCPMC7036036
OpenAlexW2995978565

What OpenQuestion holds

Textmetadata
LicenceTDM
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.