Evidence map›Paper›PMID 32664340›Full record

ArticleCells2020

Soluble St2 Induces Cardiac Fibroblast Activation and Collagen Synthesis via Neuropilin-1.

Lara Matilla, Vanessa Arrieta, Eva Jover, Amaia Garcia-Peña, Ernesto Martinez-Martinez, Rafael Sadaba, Virginia Alvarez, Adela Navarro, Amaya Fernandez-Celis, Alicia Gainza and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Neuropilin (NRPs) Related Pathological Conditions and Their Modulators.International journal of molecular sciences · 2022
    Review
  10. Article
  11. Article
  12. Interference of LPSCells · 2021
    Article
  13. Article
  14. Article
  15. Article
  16. Article
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

15 authors at 2 institutions in 2 countries.

Lara MatillaNavarrabiomed, Complejo Hospitalario de Navarra (CHN), Universidad Pública de Navarra (UPNA), IdiSNA, 31008 Pamplona, Spain.
Vanessa ArrietaNavarrabiomed, Complejo Hospitalario de Navarra (CHN), Universidad Pública de Navarra (UPNA), IdiSNA, 31008 Pamplona, Spain.
Eva JoverNavarrabiomed, Complejo Hospitalario de Navarra (CHN), Universidad Pública de Navarra (UPNA), IdiSNA, 31008 Pamplona, Spain.
Amaia Garcia-PeñaNavarrabiomed, Complejo Hospitalario de Navarra (CHN), Universidad Pública de Navarra (UPNA), IdiSNA, 31008 Pamplona, Spain.
Ernesto Martinez-MartinezNavarrabiomed, Complejo Hospitalario de Navarra (CHN), Universidad Pública de Navarra (UPNA), IdiSNA, 31008 Pamplona, Spain.ORCID 0000-0002-3011-2041
Rafael SadabaNavarrabiomed, Complejo Hospitalario de Navarra (CHN), Universidad Pública de Navarra (UPNA), IdiSNA, 31008 Pamplona, Spain.ORCID 0000-0003-3776-4744
Virginia AlvarezNavarrabiomed, Complejo Hospitalario de Navarra (CHN), Universidad Pública de Navarra (UPNA), IdiSNA, 31008 Pamplona, Spain.
Adela NavarroNavarrabiomed, Complejo Hospitalario de Navarra (CHN), Universidad Pública de Navarra (UPNA), IdiSNA, 31008 Pamplona, Spain.
Amaya Fernandez-CelisNavarrabiomed, Complejo Hospitalario de Navarra (CHN), Universidad Pública de Navarra (UPNA), IdiSNA, 31008 Pamplona, Spain.
Alicia GainzaNavarrabiomed, Complejo Hospitalario de Navarra (CHN), Universidad Pública de Navarra (UPNA), IdiSNA, 31008 Pamplona, Spain.
Enrique SantamariaProteored-ISCIII, Proteomics Unit, Navarrabiomed, Institute for Health Research, Universidad Pública de Navarra, IdiSNA, 31008 Pamplona, Spain.ORCID 0000-0001-8046-8102
Joaquín Fernandez-IrigoyenProteored-ISCIII, Proteomics Unit, Navarrabiomed, Institute for Health Research, Universidad Pública de Navarra, IdiSNA, 31008 Pamplona, Spain.ORCID 0000-0001-5072-4099
Patrick RossignolINSERM, Centre d'Investigations Cliniques-Plurithématique 1433, UMR 1116, CHRU de Nancy, French-Clinical Research Infrastructure Network (F-CRIN) INI-CRCT (Cardiovascular and Renal Clinical Trialists), Université de Lorraine, 54035 Nancy, France.
Faiez ZannadINSERM, Centre d'Investigations Cliniques-Plurithématique 1433, UMR 1116, CHRU de Nancy, French-Clinical Research Infrastructure Network (F-CRIN) INI-CRCT (Cardiovascular and Renal Clinical Trialists), Université de Lorraine, 54035 Nancy, France.
Natalia Lopez-AndresNavarrabiomed, Complejo Hospitalario de Navarra (CHN), Universidad Pública de Navarra (UPNA), IdiSNA, 31008 Pamplona, Spain.
Universidad Publica de Navarra · ESInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Circulating levels of soluble interleukin 1 receptor-like 1 (sST2) are increased in heart failure and associated with poor outcome, likely because of the activation of inflammation and fibrosis. We investigated the pathogenic role of sST2 as an inductor of cardiac fibroblasts activation and collagen synthesis. The effects of sST2 on human cardiac fibroblasts was assessed using proteomics and immunodetection approaches to evidence the upregulation of neuropilin-1 (NRP-1), a regulator of the profibrotic transforming growth factor (TGF)-β1. In parallel, sST2 increased fibroblast activation, collagen and fibrosis mediators. Pharmacological inhibition of nuclear factor-kappa B (NF-κB) restored NRP-1 levels and blocked profibrotic effects induced by sST2. In NRP-1 knockdown cells, sST2 failed to induce fibroblast activation and collagen synthesis. Exogenous NRP-1 enhanced cardiac fibroblast activation and collagen synthesis via NF-κB. In a pressure overload rat model, sST2 was elevated in association with cardiac fibrosis and was positively correlated with NRP-1 expression. Our study shows that sST2 induces human cardiac fibroblasts activation, as well as the synthesis of collagen and profibrotic molecules. These effects are mediated by NRP-1. The blockade of NF-κB restored NRP-1 expression, improving the profibrotic status induced by sST2. These results show a new pathogenic role for sST2 and its mediator, NRP-1, as cardiac fibroblast activators contributing to cardiac fibrosis.

Indexed as

AnimalsBlotting, WesternCollagenCRISPR-Cas SystemsEnzyme-Linked Immunosorbent AssayFibroblastsMaleMyocardiumNeuropilin-1NF-kappa BProteomicsRatsRats, WistarReal-Time Polymerase Chain ReactionReceptors, Interleukin-1CollagenNeuropilin-1NF-kappa BReceptors, Interleukin-1collagenfibroblast activationneuropilin-1NF-κBsST2

Identifiers

PMID32664340
PMCPMC7408622
OpenAlexW3042157917

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.