Evidence map›Paper›PMID 27151919›Full record

ArticleJournal of the American Society of Nephrology : JASN2016

Immune-Regulatory Molecule CD69 Controls Peritoneal Fibrosis.

Georgios Liappas, Guadalupe Tirma González-Mateo, Raquel Sánchez-Díaz, Juan José Lazcano, Sandra Lasarte, Adela Matesanz-Marín, Rafal Zur, Evelina Ferrantelli, Laura García Ramírez, Abelardo Aguilera and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Profibrotic MAIT17 Cells in Peritoneal Fibrosis: A New Kid on the Block?Journal of the American Society of Nephrology : JASN · 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

16 authors at 6 institutions in 2 countries.

Georgios LiappasCentro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas Universidad Autónoma de Madrid, Madrid, Spain.
Guadalupe Tirma González-MateoCentro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas Universidad Autónoma de Madrid, Madrid, Spain.
Raquel Sánchez-DíazSignaling and Inflammation Program, Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.
Juan José LazcanoSignaling and Inflammation Program, Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.
Sandra LasarteSignaling and Inflammation Program, Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.
Adela Matesanz-MarínSignaling and Inflammation Program, Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.
Rafal ZurDepartment of Immunology and Oncology, Centro Nacional de Biotecnología Consejo Superior de Investigaciones Científicas, Madrid, Spain.
Evelina FerrantelliDepartment of Molecular Cell Biology and Immunology, Vrije Universiteit University Medical Center Vrije Universiteit Medisch Centrum, Amsterdam, The Netherlands.
Laura García RamírezMolecular Biology Unit and.
Abelardo AguileraMolecular Biology Unit and.
Elena Fernández-RuizMolecular Biology Unit and.
Robert H J BeelenDepartment of Molecular Cell Biology and Immunology, Vrije Universiteit University Medical Center Vrije Universiteit Medisch Centrum, Amsterdam, The Netherlands.
Rafael SelgasNephrology Department, Hospital Universitario La Paz, Instituto de Investigación Sanitaria La Paz, Madrid, Spain.
Francisco Sánchez-MadridSignaling and Inflammation Program, Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.
Pilar MartínSignaling and Inflammation Program, Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain; pmartinf@cnic.es mlcabrera@cbm.csic.es.
Manuel López-CabreraCentro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas Universidad Autónoma de Madrid, Madrid, Spain; pmartinf@cnic.es mlcabrera@cbm.csic.es.
Spanish National Centre for Cardiovascular Research · ESConsejo Superior de Investigaciones Científicas · ESVrije Universiteit Amsterdam · NLCentro de Biología Molecular Severo Ochoa · ESHospital Universitario La Paz · ESUniversidad Autónoma de Madrid · ES

Funding

European Research Council 294340
6 · The paper itself

Abstract

Patients with ESRD undergoing peritoneal dialysis develop progressive peritoneal fibrosis, which may lead to technique failure. Recent data point to Th17-mediated inflammation as a key contributor in peritoneal damage. The leukocyte antigen CD69 modulates the setting and progression of autoimmune and inflammatory diseases by controlling the balance between Th17 and regulatory T cells (Tregs). However, the relevance of CD69 in tissue fibrosis remains largely unknown. Thus, we explored the role of CD69 in fibroproliferative responses using a mouse model of peritoneal fibrosis induced by dialysis fluid exposure under either normal or uremic status. We found that cd69

Indexed as

AnimalsAntigens, CDAntigens, Differentiation, T-LymphocyteCD69 AntigensFemaleLectins, C-TypeMicePeritoneal FibrosisTh17 CellsAntigens, CDAntigens, Differentiation, T-LymphocyteCD69 AntigensLectins, C-TypeChronic inflammationdialysisfibrosisImmunology and pathology

Identifiers

PMID27151919
PMCPMC5118477
OpenAlexW2346495881

What OpenQuestion holds

Textmetadata
LicenceTDM
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.