Evidence map›Paper›PMID 37047810›Full record

ReviewInternational journal of molecular sciences2023

The Different Pathways of Epicardial Adipose Tissue across the Heart Failure Phenotypes: From Pathophysiology to Therapeutic Target.

Valentina A Rossi, Martin Gruebler, Luca Monzo, Alessandro Galluzzo, Matteo Beltrami

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

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
8.1field-weighted citation impact, top 2% 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

26 citing papers in PubMed, 38 citations in OpenAlex.

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  10. Role of epicardial adipose tissue in heart failure with preserved ejection fraction: An emerging molecular mechanism and therapeutic potential.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2025
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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

5 authors at 4 institutions in 4 countries.

Valentina A RossiUniversity Heart Center, Department of Cardiology, University Hospital of Zurich, 8091 Zurich, Switzerland.ORCID 0000-0001-9235-6597
Martin GrueblerRegional Hospital Neustadt, 2700 Wiener Neustadt, Austria.
Luca MonzoCentre d'Investigations Cliniques Plurithématique 1433 and Inserm U1116, Université de Lorraine, CHRU Nancy, FCRIN INI-CRCT (Cardiovascular and Renal Clinical Trialists), 54035 Nancy, France.ORCID 0000-0003-2958-943X
Alessandro GalluzzoCardiology Unit, Santa Croce Hospital, Moncalieri, 10024 Turin, Italy.ORCID 0000-0003-2803-6761
Matteo BeltramiAzienda USL Toscana Centro, Cardiology Unit, San Giovanni di Dio Hospital, 50143 Florence, Italy.ORCID 0000-0001-7161-3224
Azienda Usl Toscana Centro · ITInserm · FRSigmund Freud Privatuniversität Wien · ATUniversity Hospital of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epicardial adipose tissue (EAT) is an endocrine and paracrine organ constituted by a layer of adipose tissue directly located between the myocardium and visceral pericardium. Under physiological conditions, EAT exerts protective effects of brown-like fat characteristics, metabolizing excess fatty acids, and secreting anti-inflammatory and anti-fibrotic cytokines. In certain pathological conditions, EAT acquires a proatherogenic transcriptional profile resulting in increased synthesis of biologically active adipocytokines with proinflammatory properties, promoting oxidative stress, and finally causing endothelial damage. The role of EAT in heart failure (HF) has been mainly limited to HF with preserved ejection fraction (HFpEF) and related to the HFpEF obese phenotype. In HFpEF, EAT seems to acquire a proinflammatory profile and higher EAT values have been related to worse outcomes. Less data are available about the role of EAT in HF with reduced ejection fraction (HFrEF). Conversely, in HFrEF, EAT seems to play a nutritive role and lower values may correspond to the expression of a catabolic, adverse phenotype. As of now, there is evidence that the beneficial systemic cardiovascular effects of sodium-glucose cotransporter-2 receptors-inhibitors (SGLT2-i) might be partially mediated by inducing favorable modifications on EAT. As such, EAT may represent a promising target organ for the development of new drugs to improve cardiovascular prognosis. Thus, an approach based on detailed phenotyping of cardiac structural alterations and distinctive biomolecular pathways may change the current scenario, leading towards a precision medicine model with specific therapeutic targets considering different individual profiles. The aim of this review is to summarize the current knowledge about the biomolecular pathway of EAT in HF across the whole spectrum of ejection fraction, and to describe the potential of EAT as a therapeutic target in HF.

Indexed as

Heart FailureAdipose TissueHumansPericardiumPhenotypeStroke Volumebiomolecular pathwayscardiovascular diseaseepicardial adipose tissueheart failure

Identifiers

PMID37047810
PMCPMC10095298
OpenAlexW4362668003

What OpenQuestion holds

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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.