Evidence map›Paper›PMID 28926607›Full record

ArticlePloS one2017

The novel mineralocorticoid receptor antagonist finerenone attenuates neointima formation after vascular injury.

Jochen Dutzmann, Robert-Jonathan Musmann, Marco Haertlé, Jan-Marcus Daniel, Kristina Sonnenschein, Andreas Schäfer, Peter Kolkhof, Johann Bauersachs, Daniel G Sedding

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
2.3field-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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
  2. Finerenone in People with CKD, Type 2 Diabetes, and History of Nephrectomy.Clinical journal of the American Society of Nephrology : CJASN · 2026
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  11. Mineralocorticoid receptor antagonism attenuates arteriovenous fistula stenosis by modulating the phenotype of vascular smooth muscle cells.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025
    Article
  12. Review
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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

9 authors at 2 institutions in 1 country.

Jochen DutzmannDept. of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.ORCID http://orcid.org/0000-0003-1406-2221
Robert-Jonathan MusmannDept. of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Marco HaertléDept. of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Jan-Marcus DanielDept. of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Kristina SonnenscheinDept. of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Andreas SchäferDept. of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Peter KolkhofGlobal Drug Discovery, Cardiology Research, Bayer AG, Wuppertal, Germany.
Johann BauersachsDept. of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Daniel G SeddingDept. of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Medizinische Hochschule Hannover · DEBayer (Germany) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe novel nonsteroidal mineralocorticoid receptor (MR) antagonist finerenone holds promise to be safe and efficient in the treatment of patients with heart failure and/or chronic kidney disease. However, its effects on vascular function remain elusive. PURPOSE: The aim of this study was to determine the functional effect of selective MR antagonism by finerenone in vascular cells in vitro and the effect on vascular remodeling following acute vascular injury in vivo. METHODS AND

resultsIn vitro, finerenone dose-dependently reduced aldosterone-induced smooth muscle cell (SMC) proliferation, as quantified by BrdU incorporation, and prevented aldosterone-induced endothelial cell (EC) apoptosis, as measured with a flow cytometry based caspase 3/7 activity assay. In vivo, oral application of finerenone resulted in an accelerated re-endothelialization 3 days following electric injury of the murine carotid artery. Furthermore, finerenone treatment inhibited intimal and medial cell proliferation following wire-induced injury of the murine femoral artery 10 days following injury and attenuated neointimal lesion formation 21 days following injury.

conclusionFinerenone significantly reduces apoptosis of ECs and simultaneously attenuates SMC proliferation, resulting in accelerated endothelial healing and reduced neointima formation of the injured vessels. Thus, finerenone appears to provide favorable vascular effects through restoring vascular integrity and preventing adverse vascular remodeling.

Indexed as

AldosteroneAnimalsApoptosisCarotid ArteriesCarotid Artery InjuriesCell LineCell ProliferationDisease Models, AnimalHumansHuman Umbilical Vein Endothelial CellsLeukocytesMaleMiceMice, Inbred C57BLMineralocorticoid Receptor AntagonistsMuscle, Smooth, VascularAldosteronefinerenoneMineralocorticoid Receptor AntagonistsNaphthyridines

Identifiers

PMID28926607
PMCPMC5605005
OpenAlexW2756117677

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.