Evidence map›Paper›PMID 32731636›Full record

ArticleInternational journal of molecular sciences2020

Beneficial Effects of Mineralocorticoid Receptor Antagonism on Myocardial Fibrosis in an Experimental Model of the Myxomatous Degeneration of the Mitral Valve.

Jaime Ibarrola, Mattie Garaikoetxea, Amaia Garcia-Peña, Lara Matilla, Eva Jover, Benjamin Bonnard, Maria Cuesta, Amaya Fernández-Celis, Frederic Jaisser, Natalia López-Andrés

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.8field-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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Mineralocorticoid receptor antagonism for non-diabetic kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025
    Review
  4. Article
  5. Review
  6. Signaling Pathways and Potential Therapeutic Strategies in Cardiac Fibrosis.International journal of molecular sciences · 2023
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
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 2 institutions in 2 countries.

Jaime IbarrolaCardiovascular Translational Research, Navarrabiomed (Miguel Servet Foundation), Instituto de Investigación Sanitaria de Navarra (IdiSNA), 31008 Pamplona, Spain.ORCID 0000-0003-0604-9289
Mattie GaraikoetxeaCardiovascular Translational Research, Navarrabiomed (Miguel Servet Foundation), Instituto de Investigación Sanitaria de Navarra (IdiSNA), 31008 Pamplona, Spain.ORCID 0000-0001-7656-4046
Amaia Garcia-PeñaCardiovascular Translational Research, Navarrabiomed (Miguel Servet Foundation), Instituto de Investigación Sanitaria de Navarra (IdiSNA), 31008 Pamplona, Spain.
Lara MatillaCardiovascular Translational Research, Navarrabiomed (Miguel Servet Foundation), Instituto de Investigación Sanitaria de Navarra (IdiSNA), 31008 Pamplona, Spain.
Eva JoverCardiovascular Translational Research, Navarrabiomed (Miguel Servet Foundation), Instituto de Investigación Sanitaria de Navarra (IdiSNA), 31008 Pamplona, Spain.
Benjamin BonnardCentre de Recherche des Cordeliers, INSERM, Sorbonne Université, USPC, Université Paris Descartes, Université Paris Diderot, 75013 Paris, France.ORCID 0000-0002-1746-9580
Maria CuestaCardiovascular Translational Research, Navarrabiomed (Miguel Servet Foundation), Instituto de Investigación Sanitaria de Navarra (IdiSNA), 31008 Pamplona, Spain.
Amaya Fernández-CelisCardiovascular Translational Research, Navarrabiomed (Miguel Servet Foundation), Instituto de Investigación Sanitaria de Navarra (IdiSNA), 31008 Pamplona, Spain.
Frederic JaisserCentre de Recherche des Cordeliers, INSERM, Sorbonne Université, USPC, Université Paris Descartes, Université Paris Diderot, 75013 Paris, France.
Natalia López-AndrésCardiovascular Translational Research, Navarrabiomed (Miguel Servet Foundation), Instituto de Investigación Sanitaria de Navarra (IdiSNA), 31008 Pamplona, Spain.
Navarre Institute of Health Research · ESInserm · FR

Funding

Agence Nationale de la Recherche ANR- 16-CE14-0021-01Fight-HF Avenir Investment Program ANR-15-RHUS-0004FP7-funded COST ADMIRE network BM1301Instituto de Salud Carlos III Fondo de Investigaciones Sanitarias [PI18/01875],Instituto de Salud Carlos III Miguel Servet contract CP13/00221 from the "Instituto de Salud Carlos III-FEDER"Instituto de Salud Carlos III PhD grantInstituto de Salud Carlos III sara borrellRegion Ile de France ARDoc a PhD grant
6 · The paper itself

Abstract

Mitral valve prolapse (MVP) patients develop myocardial fibrosis that is not solely explained by volume overload, but the pathophysiology has not been defined. Mineralocorticoid receptor antagonists (MRAs) improve cardiac function by decreasing cardiac fibrosis in other heart diseases. We examined the role of MRA in myocardial fibrosis associated with myxomatous degeneration of the mitral valve. Myocardial fibrosis has been analyzed in a mouse model of mitral valve myxomatous degeneration generated by pharmacological treatment with Nordexfenfluramine (NDF) in the presence of the MRA spironolactone. In vitro, adult human cardiac fibroblasts were treated with NDF and spironolactone. In an experimental mouse, MRA treatment reduced interstitial/perivascular fibrosis and collagen type I deposition. MRA administration blunted NDF-induced cardiac expression of vimentin and the profibrotic molecules galectin-3/cardiotrophin-1. In parallel, MRA blocked the increase in cardiac non-fibrillar proteins such as fibronectin, aggrecan, decorin, lumican and syndecan-4. The following effects are blocked by MRA: in vitro, in adult human cardiac fibroblasts, NDF-treatment-induced myofibroblast activation, collagen type I and proteoglycans secretion. Our findings demonstrate, for the first time, the contribution of the mineralocorticoid receptor (MR) to the development of myocardial fibrosis associated with mitral valve myxomatous degeneration. MRA could be a therapeutic approach to reduce myocardial fibrosis associated with MVP.

Indexed as

AnimalsDisease Models, AnimalFibroblastsFibrosisGene Expression RegulationHumansMaleMiceMineralocorticoid Receptor AntagonistsMitral Valve ProlapseMuscle ProteinsMyocardiumReceptors, MineralocorticoidMineralocorticoid Receptor AntagonistsMuscle ProteinsReceptors, Mineralocorticoidcardiac fibrosiscollagenmineralocorticoid receptor antagonistmyxomatous degenerationproteoglycans

Identifiers

PMID32731636
PMCPMC7432373
OpenAlexW3046052691

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.