Evidence map›Paper›PMID 40898655›Full record

Observational studyESC heart failure2025

A pilot study on DNA methylation changes for non-invasive molecular diagnostics in heart failure.

Giuditta Benincasa, Francesco Cacciatore, Mark E Pepin, Francesco Curcio, Rosaria Chiappetti, Adam R Wende, Enrico Coscioni, Claudio Napoli

Registry-linked trialAbstract readObservational Study
In one paragraph

Observational study in ESC heart failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05475028 (Network Medicine Approaches to Classify Patients Suffering Heart Failure in Relation to Left Ventricle Ejection Fraction), which is not on this map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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.

NCT05475028 completednot on this map

Network Medicine Approaches to Classify Patients Suffering Heart Failure in Relation to Left Ventricle Ejection Fraction (HFpEF, HFmrEF, HFrEF) by Circulating CD4+ T Cell-derived DNA Methylation Signatures, Clinical Data, and Point-of-care Risk Calculators

TypeobservationalSponsorUniversity of Campania Luigi VanvitelliRan2021 to 2022Enrolled60ConditionsHeart Failure, Diastolic, Heart Failure, Systolic, Pulmonary Hypertension, Atrial FibrillationArmsRRBS
3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Observational
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

8 authors.

Giuditta BenincasaDepartment of Advanced Medical and Surgical Sciences (DAMSS), University of Campania 'Luigi Vanvitelli', Naples, Italy.ORCID https://orcid.org/0000-0002-7552-3522
Francesco CacciatoreDepartment of Translational Medical Sciences, University of Naples 'Federico II', Naples, Italy.
Mark E PepinStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, California, USA.
Francesco CurcioDepartment of Translational Medical Sciences, University of Naples 'Federico II', Naples, Italy.
Rosaria ChiappettiDepartment of Translational Medical Sciences, University of Naples 'Federico II', Naples, Italy.
Adam R WendeDivision of Molecular and Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Enrico CoscioniDivision of Cardiac Surgery, AOU San Giovanni di Dio e Ruggi d'Aragona, Salerno, Italy.
Claudio NapoliDepartment of Advanced Medical and Surgical Sciences (DAMSS), University of Campania 'Luigi Vanvitelli', Naples, Italy.

Funding

Ministry of University and Research (MUR) PNRR-AGE-IT-PE0000015Ministry of University and Research (MUR) PRIN2020XMLP45
6 · The paper itself

Abstract

aimsThe current therapeutic approach to ischaemic (IsHF) and non-ischaemic (NIsHF) heart failure (HF) mainly overlooks the underlying aetiology owing to a lack knowledge of the differential molecular pathways that contribute to HF with reduced ejection fraction (HFrEF). Alterations in myocardial DNA methylation levels have been identified as potential biomarkers for HF irrespective of its aetiology. Due to the limited availability of cardiac tissues in clinics, our goal is to determine if DNA methylation changes in circulating CD4 METHODS AND

resultsWe performed a post hoc network-oriented analysis of the original PRESMET clinical trial dataset (NCT05475028). Integrating epigenomic data obtained with the high-resolution reduced representation bisulfite sequencing (RRBS) platform and the left-ventricle interactome (protein-protein interaction map) we identified six differentially methylated CpG positions (DMPs), which were able to distinguish IsHF (n = 8) versus NIsHF (n = 4) patients with an area under the curve (AUC) > 0.8. Network-oriented DMPs were significantly hypomethylated in IsHF versus NIsHF and annotated to six genes, namely, cytoskeleton-associated protein 4 (CKAP4), carnitine palmitoyltransferase 1A (CPT1A), eukaryotic translation initiation factor 2 subunit beta (EIF2S2), spectrin beta (SPTB), synaptotagmin 6 (SYT6) and RAB11 family interacting protein 1 (RAB11FIP1) (P < 0.05). We found that the CD4

conclusionsWe demonstrate that circulating CD4

Indexed as

DNADNA MethylationHeart FailureStroke VolumeAgedBiomarkersFemaleHumansMaleMiddle AgedPilot ProjectsVentricular RemodelingBiomarkersDNAbiomarkersCD4+ T cellsDNA methylationheart failureinteractomenetwork medicineRRBS

Identifiers

PMID40898655
PMCPMC12719838

What Socratic holds

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LicenceCC BY
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Registered trials

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.