Evidence map›Paper›PMID 35008960›Full record

SynthesisInternational journal of molecular sciences2022

Impact of Uremic Toxins on Endothelial Dysfunction in Chronic Kidney Disease: A Systematic Review.

Eva Harlacher, Julia Wollenhaupt, Constance C F M J Baaten, Heidi Noels

Open access · goldAbstract readSystematic Review
In one paragraph

Synthesis in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed, 3 pooled it
13.3field-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

108 citing papers in PubMed, 3 syntheses or guidelines pooled it, 114 citations in OpenAlex.

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  11. A Vein Attempt? Experimental Models for Arteriovenous Fistula Research.Cardiovascular engineering and technology · 2026
    Review
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48 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

4 authors at 2 institutions in 2 countries.

Eva HarlacherInstitute for Molecular Cardiovascular Research, University Hospital Aachen, Rheinisch-Westfälische Technische Hochschule Aachen University, 52074 Aachen, Germany.
Julia WollenhauptInstitute for Molecular Cardiovascular Research, University Hospital Aachen, Rheinisch-Westfälische Technische Hochschule Aachen University, 52074 Aachen, Germany.
Constance C F M J BaatenInstitute for Molecular Cardiovascular Research, University Hospital Aachen, Rheinisch-Westfälische Technische Hochschule Aachen University, 52074 Aachen, Germany.
Heidi NoelsInstitute for Molecular Cardiovascular Research, University Hospital Aachen, Rheinisch-Westfälische Technische Hochschule Aachen University, 52074 Aachen, Germany.ORCID 0000-0003-3053-6984
Maastricht University · NLUniversitätsklinikum Aachen · DE

Funding

Deutsche Forschungsgemeinschaft ID 322900939Deutsche Forschungsgemeinschaft ID 403224013Else Kröner-Fresenius-Stiftung Project 2020_EKEA.60European Union's Horizon 2020 research and innovation programme under the Marie Skłodow-ska- Curie grant agreement No 860329RWTH Aachen University 105/20
6 · The paper itself

Abstract

Patients with chronic kidney disease (CKD) are at a highly increased risk of cardiovascular complications, with increased vascular inflammation, accelerated atherogenesis and enhanced thrombotic risk. Considering the central role of the endothelium in protecting from atherogenesis and thrombosis, as well as its cardioprotective role in regulating vasorelaxation, this study aimed to systematically integrate literature on CKD-associated endothelial dysfunction, including the underlying molecular mechanisms, into a comprehensive overview. Therefore, we conducted a systematic review of literature describing uremic serum or uremic toxin-induced vascular dysfunction with a special focus on the endothelium. This revealed 39 studies analyzing the effects of uremic serum or the uremic toxins indoxyl sulfate, cyanate, modified LDL, the advanced glycation end products N-carboxymethyl-lysine and N-carboxyethyl-lysine, p-cresol and p-cresyl sulfate, phosphate, uric acid and asymmetric dimethylarginine. Most studies described an increase in inflammation, oxidative stress, leukocyte migration and adhesion, cell death and a thrombotic phenotype upon uremic conditions or uremic toxin treatment of endothelial cells. Cellular signaling pathways that were frequently activated included the ROS, MAPK/NF-κB, the Aryl-Hydrocarbon-Receptor and RAGE pathways. Overall, this review provides detailed insights into pathophysiological and molecular mechanisms underlying endothelial dysfunction in CKD. Targeting these pathways may provide new therapeutic strategies reducing increased the cardiovascular risk in CKD.

Indexed as

Disease SusceptibilityAnimalsApoptosisBiomarkersCardiovascular DiseasesEndoplasmic Reticulum StressEndothelial CellsEndothelium, VascularHumansNitric OxideOxidative StressProtein Processing, Post-TranslationalRenal Insufficiency, ChronicSignal TransductionUremic ToxinsBiomarkersNitric OxideUremic Toxinscardiovascular diseasechronic kidney diseaseendothelial cellsendothelial dysfunctionuremic toxinsvascular dysfunctionvascular pathophysiology

Identifiers

PMID35008960
PMCPMC8745705
OpenAlexW4205690052

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.