Evidence map›Paper›PMID 24599232›Full record

ReviewToxins2014

The aryl hydrocarbon receptor-activating effect of uremic toxins from tryptophan metabolism: a new concept to understand cardiovascular complications of chronic kidney disease.

Marion Sallée, Laetitia Dou, Claire Cerini, Stéphane Poitevin, Philippe Brunet, Stéphane Burtey

Open access · goldAbstract readReview
In one paragraph

Review in Toxins, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
136citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 3% 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

136 citing papers in PubMed, 1 synthesis or guideline pooled it, 249 citations in OpenAlex.

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76 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

6 authors at 1 institution in 1 country.

Marion SalléeAix Marseille Université, Inserm, VRCM, UMR_S 1076, Marseille13005, France. marionsallee@yahoo.fr.
Laetitia DouAix Marseille Université, Inserm, VRCM, UMR_S 1076, Marseille13005, France. laetitia.dou@univ-amu.fr.
Claire CeriniAix Marseille Université, Inserm, VRCM, UMR_S 1076, Marseille13005, France. claire.cerini@univ-amu.fr.
Stéphane PoitevinAix Marseille Université, Inserm, VRCM, UMR_S 1076, Marseille13005, France. stephane.poitevin@univ-amu.fr.
Philippe BrunetAix Marseille Université, Inserm, VRCM, UMR_S 1076, Marseille13005, France. drphilippe.brunet@outlook.com.
Stéphane BurteyAix Marseille Université, Inserm, VRCM, UMR_S 1076, Marseille13005, France. stephane.burtey@ap-hm.fr.
Inserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients with chronic kidney disease (CKD) have a higher risk of cardiovascular diseases and suffer from accelerated atherosclerosis. CKD patients are permanently exposed to uremic toxins, making them good candidates as pathogenic agents. We focus here on uremic toxins from tryptophan metabolism because of their potential involvement in cardiovascular toxicity: indolic uremic toxins (indoxyl sulfate, indole-3 acetic acid, and indoxyl-β-d-glucuronide) and uremic toxins from the kynurenine pathway (kynurenine, kynurenic acid, anthranilic acid, 3-hydroxykynurenine, 3-hydroxyanthranilic acid, and quinolinic acid). Uremic toxins derived from tryptophan are endogenous ligands of the transcription factor aryl hydrocarbon receptor (AhR). AhR, also known as the dioxin receptor, interacts with various regulatory and signaling proteins, including protein kinases and phosphatases, and Nuclear Factor-Kappa-B. AhR activation by 2,3,7,8-tetrachlorodibenzo-p-dioxin and some polychlorinated biphenyls is associated with an increase in cardiovascular disease in humans and in mice. In addition, this AhR activation mediates cardiotoxicity, vascular inflammation, and a procoagulant and prooxidant phenotype of vascular cells. Uremic toxins derived from tryptophan have prooxidant, proinflammatory, procoagulant, and pro-apoptotic effects on cells involved in the cardiovascular system, and some of them are related with cardiovascular complications in CKD. We discuss here how the cardiovascular effects of these uremic toxins could be mediated by AhR activation, in a "dioxin-like" effect.

Indexed as

AnimalsCardiovascular DiseasesEndothelium, VascularHumansLeukocytesOxidative StressReceptors, Aryl HydrocarbonRenal Insufficiency, ChronicToxins, BiologicalTryptophanUremiaReceptors, Aryl HydrocarbonToxins, BiologicalTryptophan

Identifiers

PMID24599232
PMCPMC3968369
OpenAlexW2064094137

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.