Evidence map›Paper›PMID 26240279›Full record

ArticleMolecular and cellular biology2015

Immunosuppression-Independent Role of Regulatory T Cells against Hypertension-Driven Renal Dysfunctions.

Salvatore Fabbiano, Mauricio Menacho-Márquez, Javier Robles-Valero, Miguel Pericacho, Adela Matesanz-Marín, Carmen García-Macías, María A Sevilla, M J Montero, Balbino Alarcón, José M López-Novoa and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.1field-weighted citation impact, top 10% 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

27 citing papers in PubMed, 37 citations in OpenAlex.

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  15. Association of the ENPP1/ENTPD1 Polymorphisms in Hemodialysis Patients.International journal of general medicine · 2021
    Article
  16. Actions of immune cells in the hypertensive kidney.Current opinion in nephrology and hypertension · 2020
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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

12 authors at 4 institutions in 1 country.

Salvatore FabbianoCentro de Investigación del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-University of Salamanca, Salamanca, Spain Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-University of Salamanca, Salamanca, Spain.
Mauricio Menacho-MárquezCentro de Investigación del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-University of Salamanca, Salamanca, Spain Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-University of Salamanca, Salamanca, Spain.
Javier Robles-ValeroCentro de Investigación del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-University of Salamanca, Salamanca, Spain Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-University of Salamanca, Salamanca, Spain.
Miguel PericachoDepartamento de Fisiología y Farmacología, University of Salamanca, Salamanca, Spain.
Adela Matesanz-MarínCentro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.
Carmen García-MacíasCentro de Investigación del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-University of Salamanca, Salamanca, Spain Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-University of Salamanca, Salamanca, Spain.
María A SevillaDepartamento de Fisiología y Farmacología, University of Salamanca, Salamanca, Spain.
M J MonteroDepartamento de Fisiología y Farmacología, University of Salamanca, Salamanca, Spain.
Balbino AlarcónCentro de Biología Molecular Severo Ochoa, CSIC, Madrid, Spain.
José M López-NovoaDepartamento de Fisiología y Farmacología, University of Salamanca, Salamanca, Spain.
Pilar MartínCentro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.
Xosé R BusteloCentro de Investigación del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-University of Salamanca, Salamanca, Spain Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-University of Salamanca, Salamanca, Spain xbustelo@usal.es.ORCID http://orcid.org/0000-0001-9398-6072
Consejo Superior de Investigaciones Científicas · ESUniversidad de Salamanca · ESSpanish National Centre for Cardiovascular Research · ESCentro de Biología Molecular Severo Ochoa · ES

Funding

Worldwide Cancer Research 14-1248
6 · The paper itself

Abstract

Hypertension-associated cardiorenal diseases represent one of the heaviest burdens for current health systems. In addition to hemodynamic damage, recent results have revealed that hematopoietic cells contribute to the development of these diseases by generating proinflammatory and profibrotic environments in the heart and kidney. However, the cell subtypes involved remain poorly characterized. Here we report that CD39(+) regulatory T (TREG) cells utilize an immunosuppression-independent mechanism to counteract renal and possibly cardiac damage during angiotensin II (AngII)-dependent hypertension. This mechanism relies on the direct apoptosis of tissue-resident neutrophils by the ecto-ATP diphosphohydrolase activity of CD39. In agreement with this, experimental and genetic alterations in TREG/TH cell ratios have a direct impact on tissue-resident neutrophil numbers, cardiomyocyte hypertrophy, cardiorenal fibrosis, and, to a lesser extent, arterial pressure elevation during AngII-driven hypertension. These results indicate that TREG cells constitute a first protective barrier against hypertension-driven tissue fibrosis and, in addition, suggest new therapeutic avenues to prevent hypertension-linked cardiorenal diseases.

Indexed as

Angiotensin IIAnimalsAntigens, CDApoptosisApyraseCells, CulturedFibrosisHypertensionImmune ToleranceKidneyMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMice, SCIDNeutrophilsProto-Oncogene Proteins c-vavAngiotensin IIAntigens, CDApyraseCD39 antigenProto-Oncogene Proteins c-vavVav1 protein, mouse

Identifiers

PMID26240279
PMCPMC4573708
OpenAlexW2148770155

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.