Evidence map›Paper›PMID 31694161›Full record

ReviewMolecules (Basel, Switzerland)2019

Circulating Metabolites Originating from Gut Microbiota Control Endothelial Cell Function.

Amedeo Amedei, Lucia Morbidelli

Abstract readReview
In one paragraph

Review in Molecules (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
–field-weighted citation impact
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

40 citing papers in PubMed.

  1. The Roles of Gut Microbiota in the Pathogenesis of Acute Pancreatitis.Medical science monitor : international medical journal of experimental and clinical research · 2026
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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

2 authors.

Amedeo AmedeiDepartment of Experimental and Clinical Medicine, University of Florence, Viale Pieraccini 6, 50134 Florence, Italy.ORCID 0000-0002-6797-9343
Lucia MorbidelliDepartment of Life Sciences, University of Siena, Via A. Moro 2, 53100 Siena, Italy.ORCID 0000-0001-8148-7049

Funding

Italian Ministry of Education, University and Research 2017XP72RF
6 · The paper itself

Abstract

Cardiovascular functionality strictly depends on endothelial cell trophism and proper biochemical function. Any condition (environmental, pharmacological/toxicological, physical, or neuro-humoral) that changes the vascular endothelium has great consequences for the organism's wellness and on the outcome and evolution of severe cardiovascular pathologies. Thus, knowledge of the mechanisms, both endogenous and external, that affect endothelial dysfunction is pivotal to preventing and treating these disorders. In recent decades, significant attention has been focused on gut microbiota and how these symbiotic microorganisms can influence host health and disease development. Indeed, dysbiosis has been reported to be at the base of a range of different pathologies, including pathologies of the cardiovascular system. The study of the mechanism underlying this relationship has led to the identification of a series of metabolites (released by gut bacteria) that exert different effects on all the components of the vascular system, and in particular on endothelial cells. The imbalance of factors promoting or blunting endothelial cell viability and function and angiogenesis seems to be a potential target for the development of new therapeutic interventions. This review highlights the circulating factors identified to date, either directly produced by gut microbes or resulting from the metabolism of diet derivatives as polyphenols.

Indexed as

AnimalsCardiovascular DiseasesCell SurvivalEndothelial CellsEndothelium, VascularGastrointestinal MicrobiomeHumanscardiovascular diseasesendothelial cellendothelial dysfunctiongut microbiotahypertensioninflammationmetabolitenitric oxidepolyphenolsreactive oxygen species

Identifiers

PMID31694161
PMCPMC6864778

What OpenQuestion holds

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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.