Evidence map›Paper›PMID 25012164›Full record

ArticleJournal of the American Society of Nephrology : JASN2015

A pathogenetic role for endothelin-1 in peritoneal dialysis-associated fibrosis.

Oscar Busnadiego, Jesús Loureiro-Álvarez, Pilar Sandoval, David Lagares, Javier Dotor, María Luisa Pérez-Lozano, María J López-Armada, Santiago Lamas, Manuel López-Cabrera, Fernando Rodríguez-Pascual

Open access · greenAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 37 citations in OpenAlex.

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  17. Immune-Regulatory Molecule CD69 Controls Peritoneal Fibrosis.Journal of the American Society of Nephrology : JASN · 2016
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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

10 authors at 3 institutions in 1 country.

Oscar BusnadiegoCentro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Madrid, Spain;
Jesús Loureiro-ÁlvarezCentro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Madrid, Spain; Laboratorio de Envejecimiento e Inflamación, Instituto de Investigación Biomédica, A Coruña, A Coruña, Spain; and.
Pilar SandovalCentro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Madrid, Spain;
David LagaresCentro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Madrid, Spain;
Javier DotorDigna Biotech, Madrid, Spain.
María Luisa Pérez-LozanoCentro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Madrid, Spain;
María J López-ArmadaLaboratorio de Envejecimiento e Inflamación, Instituto de Investigación Biomédica, A Coruña, A Coruña, Spain; and.
Santiago LamasCentro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Madrid, Spain;
Manuel López-CabreraCentro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Madrid, Spain;
Fernando Rodríguez-PascualCentro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Madrid, Spain; frodriguez@cbm.csic.es.
Consejo Superior de Investigaciones Científicas · ESUniversidad Autónoma de Madrid · ESCentro de Biología Molecular Severo Ochoa · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In patients undergoing peritoneal dialysis (PD), chronic exposure to nonphysiologic PD fluids elicits low-grade peritoneal inflammation, leading to fibrosis and angiogenesis. Phenotype conversion of mesothelial cells into myofibroblasts, the so-called mesothelial-to-mesenchymal transition (MMT), significantly contributes to the peritoneal dysfunction related to PD. A number of factors have been described to induce MMT in vitro and in vivo, of which TGF-β1 is probably the most important. The vasoconstrictor peptide endothelin-1 (ET-1) is a transcriptional target of TGF-β1 and mediates excessive scarring and fibrosis in several tissues. This work studied the contribution of ET-1 to the development of peritoneal damage and failure in a mouse model of PD. ET-1 and its receptors were expressed in the peritoneal membrane and upregulated on PD fluid exposure. Administration of an ET receptor antagonist, either bosentan or macitentan, markedly attenuated PD-induced MMT, fibrosis, angiogenesis, and peritoneal functional decline. Adenovirus-mediated overexpression of ET-1 induced MMT in human mesothelial cells in vitro and promoted the early cellular events associated with peritoneal dysfunction in vivo. Notably, TGF-β1-blocking peptides prevented these actions of ET-1. Furthermore, a positive reciprocal relationship was observed between ET-1 expression and TGF-β1 expression in human mesothelial cells. These results strongly support a role for an ET-1/TGF-β1 axis as an inducer of MMT and subsequent peritoneal damage and fibrosis, and they highlight ET-1 as a potential therapeutic target in the treatment of PD-associated dysfunction.

Indexed as

AdenoviridaeAnimalsCells, CulturedEndothelin-1Epithelial CellsEpitheliumFemaleFibrosisGene Transfer TechniquesHumansMiceMice, Inbred C57BLPeritoneal DialysisPeritoneal FibrosisPeritoneumPhenotypeEndothelin-1Transforming Growth Factor beta1endothelin-1fibrosisperitoneal dialysisTGF-β1ultrafiltration

Identifiers

PMID25012164
PMCPMC4279729
OpenAlexW2099094020

What OpenQuestion holds

Textmetadata
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.