Evidence map›Paper›PMID 35455943›Full record

ArticleCells2022

The Effect of Mineralocorticoid Receptor 3 Antagonists on Anti-Inflammatory and Anti-Fatty Acid Transport Profile in Patients with Heart Failure.

Xiaoran Fu, Cristina Almenglo, Ángel Luis Fernandez, José Manuel Martínez-Cereijo, Diego Iglesias-Alvarez, Darío Duran-Muñoz, Tomás García-Caballero, Jose Ramón Gonzalez-Juanatey, Moises Rodriguez-Mañero, Sonia Eiras

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

8 citing papers in PubMed, 18 citations in OpenAlex.

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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

10 authors at 1 institution in 1 country.

Xiaoran FuTranslational Cardiology Group, Health Research Institute, 15706 Santiago de Compostela, Spain.
Cristina AlmengloCardiology Group, Health Research Institute, University Hospital of Santiago de Compostela, 15706 Santiago de Compostela, Spain.ORCID 0000-0003-2661-4265
Ángel Luis FernandezHeart Surgery Department, University Hospital of Santiago de Compostela, 15706 Santiago de Compostela, Spain.
José Manuel Martínez-CereijoHeart Surgery Department, University Hospital of Santiago de Compostela, 15706 Santiago de Compostela, Spain.ORCID 0000-0001-8976-3159
Diego Iglesias-AlvarezCardiology Group, Health Research Institute, University Hospital of Santiago de Compostela, 15706 Santiago de Compostela, Spain.
Darío Duran-MuñozHeart Surgery Department, University Hospital of Santiago de Compostela, 15706 Santiago de Compostela, Spain.
Tomás García-CaballeroMorphological Sciences Department, Medicine Faculty, University of Santiago de Compostela and Pathology Department, University Hospital of Santiago de Compostela, 15706 Santiago de Compostela, Spain.
Jose Ramón Gonzalez-JuanateyCardiology Group, Health Research Institute, University Hospital of Santiago de Compostela, 15706 Santiago de Compostela, Spain.ORCID 0000-0001-9681-3388
Moises Rodriguez-MañeroTranslational Cardiology Group, Health Research Institute, 15706 Santiago de Compostela, Spain.
Sonia EirasTranslational Cardiology Group, Health Research Institute, 15706 Santiago de Compostela, Spain.
Universidade de Santiago de Compostela · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epicardial fat thickness is associated with cardiovascular disease. Mineralocorticoid receptor antagonist (MRA), a pharmaceutical treatment for CVD, was found to have an effect on adipose tissue. Our aim was to analyse the main epicardial fat genesis and inflammation-involved cell markers and their regulation by risk factors and MRA. We included blood and epicardial or subcutaneous fat (EAT or SAT) from 71 patients undergoing heart surgery and blood from 66 patients with heart failure. Cell types (transcripts or proteins) were analysed by real-time polymerase chain reaction or immunohistochemistry. Plasma proteins were analysed by Luminex technology or enzyme-linked immunoassay. Our results showed an upregulation of fatty acid transporter levels after aldosterone-induced genesis. The MRA intake was the main factor associated with lower levels in epicardial fat. On the contrary, MRA upregulated the levels and its secretion of the anti-inflammatory marker intelectin 1 and reduced the proliferation of epicardial fibroblasts. Our results have shown the local MRA intake effect on fatty acid transporters and anti-inflammatory marker levels and the proliferation rate on epicardial fat fibroblasts. They suggest the role of MRA on epicardial fat genesis and remodelling in patients with cardiovascular disease. Translational perspective: the knowledge of epicardial fat genesis and its modulation by drugs might be useful for improving the treatments of cardiovascular disease.

Indexed as

Cardiovascular DiseasesHeart FailureAnti-Inflammatory AgentsBiomarkersFatty AcidsHumansMineralocorticoid Receptor AntagonistsReceptors, MineralocorticoidAnti-Inflammatory AgentsBiomarkersFatty AcidsMineralocorticoid Receptor AntagonistsReceptors, Mineralocorticoidepicardial fatparasympathetic dysfunction

Identifiers

PMID35455943
PMCPMC9027091
OpenAlexW4224220971

What Socratic 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 Socratic graph.