Evidence map›Paper›PMID 32575762›Full record

ReviewToxins2020

How do Uremic Toxins Affect the Endothelium?

Regiane Stafim da Cunha, Andressa Flores Santos, Fellype Carvalho Barreto, Andréa Emilia Marques Stinghen

Open access · goldAbstract readReview
In one paragraph

Review in Toxins, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
5.0field-weighted citation impact, top 4% 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, 61 citations in OpenAlex.

  1. Trial
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  8. Kidney-heart crosstalk: the extracellular vesicles connection.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 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

4 authors at 1 institution in 1 country.

Regiane Stafim da CunhaExperimental Nephrology Laboratory, Basic Pathology Department, Universidade Federal do Paraná, Curitiba 81531-980, Brazil.ORCID 0000-0002-7925-7698
Andressa Flores SantosExperimental Nephrology Laboratory, Basic Pathology Department, Universidade Federal do Paraná, Curitiba 81531-980, Brazil.ORCID 0000-0001-6496-4333
Fellype Carvalho BarretoInternal Medicine Department, Division of Nephrology, Universidade Federal do Paraná, Curitiba 80060-900, Brazil.ORCID 0000-0002-6394-9227
Andréa Emilia Marques StinghenExperimental Nephrology Laboratory, Basic Pathology Department, Universidade Federal do Paraná, Curitiba 81531-980, Brazil.ORCID 0000-0001-8595-5321
Universidade Federal do Paraná · BR

Funding

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - Brasil (CAPES) Finance Code 001
6 · The paper itself

Abstract

Uremic toxins can induce endothelial dysfunction in patients with chronic kidney disease (CKD). Indeed, the structure of the endothelial monolayer is damaged in CKD, and studies have shown that the uremic toxins contribute to the loss of cell-cell junctions, increasing permeability. Membrane proteins, such as transporters and receptors, can mediate the interaction between uremic toxins and endothelial cells. In these cells, uremic toxins induce oxidative stress and activation of signaling pathways, including the aryl hydrocarbon receptor (AhR), nuclear factor kappa B (NF-κB), and mitogen-activated protein kinase (MAPK) pathways. The activation of these pathways leads to overexpression of proinflammatory (e.g., monocyte chemoattractant protein-1, E-selectin) and prothrombotic (e.g., tissue factor) proteins. Uremic toxins also induce the formation of endothelial microparticles (EMPs), which can lead to the activation and dysfunction of other cells, and modulate the expression of microRNAs that have an important role in the regulation of cellular processes. The resulting endothelial dysfunction contributes to the pathogenesis of cardiovascular diseases, such as atherosclerosis and thrombotic events. Therefore, uremic toxins as well as the pathways they modulated may be potential targets for therapies in order to improve treatment for patients with CKD.

Indexed as

AnimalsCardiovascular DiseasesEndothelium, VascularHumansRenal Insufficiency, ChronicSignal TransductionToxins, BiologicalUremiaToxins, Biologicalendothelial dysfunctionendotheliumuremic toxins

Identifiers

PMID32575762
PMCPMC7354502
OpenAlexW3037818471

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.