Evidence map›Paper›PMID 31382511›Full record

ArticleToxins2019

Indoxyl Sulfate Stimulates Angiogenesis by Regulating Reactive Oxygen Species Production via CYP1B1.

Jiayi Pei, Rio Juni, Magdalena Harakalova, Dirk J Duncker, Folkert W Asselbergs, Pieter Koolwijk, Victor van Hinsbergh, Marianne C Verhaar, Michal Mokry, Caroline Cheng

Open access · goldAbstract read
In one paragraph

Article in Toxins, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Observational
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. CYP1B1 as a therapeutic target in cardio-oncology.Clinical science (London, England : 1979) · 2020
    Article
  11. Article
  12. 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

10 authors at 3 institutions in 2 countries.

Jiayi PeiDepartment of Nephrology and Hypertension, DIGD, UMC Utrecht, University of Utrecht, 3584 CX Utrecht, The Netherlands.
Rio JuniDepartment of Physiology, Amsterdam UMC, VUmc location, Amsterdam Cardiovascular Science, 1081 HV Amsterdam, The Netherlands.
Magdalena HarakalovaDepartment of Cardiology, Division Heart & Lungs, UMC Utrecht, University of Utrecht, 3584 CX Utrecht, The Netherlands.
Dirk J DunckerDepartment of Cardiology, Erasmus MC, Rotterdam, 3015 GD, The Netherlands.
Folkert W AsselbergsDepartment of Cardiology, Division Heart & Lungs, UMC Utrecht, University of Utrecht, 3584 CX Utrecht, The Netherlands.
Pieter KoolwijkDepartment of Physiology, Amsterdam UMC, VUmc location, Amsterdam Cardiovascular Science, 1081 HV Amsterdam, The Netherlands.
Victor van HinsberghDepartment of Physiology, Amsterdam UMC, VUmc location, Amsterdam Cardiovascular Science, 1081 HV Amsterdam, The Netherlands.
Marianne C VerhaarDepartment of Nephrology and Hypertension, DIGD, UMC Utrecht, University of Utrecht, 3584 CX Utrecht, The Netherlands.
Michal MokryRegenerative Medicine Utrecht, UMC Utrecht, University of Utrecht, 3584 CX Utrecht, The Netherlands.
Caroline ChengDepartment of Nephrology and Hypertension, DIGD, UMC Utrecht, University of Utrecht, 3584 CX Utrecht, The Netherlands. K.L.Cheng-2@umcutrecht.nl.
Utrecht University · NLAmsterdam Neuroscience · NLErasmus MC · NL

Funding

Department of Health
6 · The paper itself

Abstract

Indoxyl sulfate (IS) is an accumulative protein-bound uremic toxin found in patients with kidney disease. It is reported that IS impairs the vascular endothelium, but a comprehensive overview of all mechanisms active in IS-injury currently remains lacking. Here we performed RNA sequencing in human umbilical vein endothelial cells (HUVECs) after IS or control medium treatment and identified 1293 genes that were affected in a IS-induced response. Gene enrichment analysis highlighted pathways involved in altered vascular formation and cell metabolism. We confirmed these transcriptome profiles at the functional level by demonstrating decreased viability and increased cell senescence in response to IS treatment. In line with the additional pathways highlighted by the transcriptome analysis, we further could demonstrate that IS exposure of HUVECs promoted tubule formation as shown by the increase in total tubule length in a 3D HUVECs/pericytes co-culture assay. Notably, the pro-angiogenic response of IS and increased ROS production were abolished when

Indexed as

Cytochrome P-450 CYP1B1Endothelium, VascularGene Expression ProfilingHumansHuman Umbilical Vein Endothelial CellsIndicanNeovascularization, PhysiologicReactive Oxygen SpeciesSequence Analysis, RNACYP1B1 protein, humanCytochrome P-450 CYP1B1IndicanReactive Oxygen Speciesangiogenesischronic kidney diseaseCYP1B1indoxyl sulfatereactive oxygen species

Identifiers

PMID31382511
PMCPMC6723868
OpenAlexW2965099773

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.