Evidence map›Paper›PMID 30314315›Full record

ArticleToxins2018

Urea Memory: Transient Cell Exposure to Urea Causes Persistent Mitochondrial ROS Production and Endothelial Dysfunction.

Maria d'Apolito, Anna Laura Colia, Enrica Manca, Massimo Pettoello-Mantovani, Michele Sacco, Angela Bruna Maffione, Michael Brownlee, Ida Giardino

Open access · goldAbstract read
In one paragraph

Article in Toxins, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

13 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. The Multifaceted Role of Mitochondria in Angiogenesis.International journal of molecular sciences · 2025
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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

8 authors at 2 institutions in 2 countries.

Maria d'ApolitoPediatric Research Center, Department of Medical and Surgical Sciences, University of Foggia, 71122 Foggia, Italy. maria.dapolito@unifg.it.
Anna Laura ColiaDepartment of Clinical and Experimental Medicine, University of Foggia, 71122 Foggia, Italy. annalaura.colia@gmail.com.
Enrica MancaPediatric Residency Program, University of Foggia, 71122 Foggia, Italy. enricamanca@hotmail.com.
Massimo Pettoello-MantovaniPediatric Research Center, Department of Medical and Surgical Sciences, University of Foggia, 71122 Foggia, Italy. massimo.pettoellomantovani@unifg.it.
Michele SaccoDepartement of Pediatrics, Scientific Institute "Casa Sollievo della Sofferenza", University of Foggia, 71122 Foggia, Italy. m.sacco@operapadrepio.it.
Angela Bruna MaffioneDepartment of Clinical and Experimental Medicine, University of Foggia, 71122 Foggia, Italy. angelabruna.maffione@unifg.it.
Michael BrownleeDiabetes Research Center, Albert Einstein College of Medicine, New York, NY 10461, USA. Michael.Brownlee@einstein.yu.edu.
Ida GiardinoDepartment of Clinical and Experimental Medicine, University of Foggia, 71122 Foggia, Italy. ida.giardino@unifg.it.
University of Foggia · ITAlbert Einstein College of Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Urea at post-dialysis levels induces increased ROS in a number of cell types. The aim of this study was to determine whether urea-induced production of ROS remains elevated after urea is no longer present, and, if it does, to characterize its origin and effects. Human arterial endothelial cells were incubated with 20 mM urea for two days, and then cells were incubated for an additional two days in medium alone. Maximal ROS levels induced by initial urea continued at the same level despite urea being absent. These effects were prevented by either MnSOD expression or by Nox1/4 inhibition with GKT13781. Sustained urea-induced ROS caused a persistent reduction in mtDNA copy number and electron transport chain transcripts, a reduction in transcription of mitochondrial fusion proteins, an increase in mitochondrial fission proteins, and persistent expression of endothelial inflammatory markers. The SOD-catalase mimetic MnTBAP reversed each of these. These results suggest that persistent increases in ROS after cells are no long exposed to urea may play a major role in continued kidney damage and functional decline despite reduction of urea levels after dialysis.

Indexed as

Cells, CulturedEndothelial CellsHumansMitochondriaMitochondrial DynamicsReactive Oxygen SpeciesUreaReactive Oxygen SpeciesUreacardiovascular diseasechronic renal failureCRFCVDend stage renal diseaseESRDreactive oxygen speciesROSureauremic memory

Identifiers

PMID30314315
PMCPMC6215169
OpenAlexW2896806151

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.