Evidence mapPaperPMID 42074089Full record

ArticleInternational journal of molecular sciences2026

Exploring Biomarkers in Congenital Heart Disease: A Case-Control Study of ST2 in Children with Atrial Septal Defects.

Henning Clausen, Elin Friberg, Mikko Sairanen, Pia Sjöberg, Petru Liuba

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing 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.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Henning ClausenPediatric Cardiology, Children's Heart Centre, Skåne University Hospital, 221 85 Lund, Sweden.
Elin FribergPediatric Cardiology, Children's Heart Centre, Skåne University Hospital, 221 85 Lund, Sweden.ORCID 0009-0003-4147-3867
Mikko SairanenResearch and Development Division, Revvity, 20520 Turku, Finland.ORCID 0000-0002-7246-1354
Pia SjöbergDepartment of Clinical Physiology, Skåne University Hospital, 221 85 Lund, Sweden.ORCID 0000-0002-9721-2880
Petru LiubaPediatric Cardiology, Children's Heart Centre, Skåne University Hospital, 221 85 Lund, Sweden.

Funding

Region Skåne Nos. 2025-2749 and 2022-0288Swedish Heart-Lung Foundation Nos. 20241381, 20240935, 20240862, 20220737, 20220369 and 20210399Swedish Research Council No. 202202757Swedish Society of Medicine No.100611
6 · The paper itself

Abstract

Soluble growth stimulation protein form of interleukin-1 receptor-like 1 (ST2) may signal myocardial stress, and elevated ST2 blood levels are associated with adverse outcomes in adult heart disease. Data on ST2 in children with congenital heart disease (CHD) is limited. This study explored ST2 in newborns and older children with atrial septal defect (ASD), as this represents a common CHD type that remains clinically challenging to recognize in childhood with slowly evolving symptoms. A case-control study was carried out in newborn ASD cases versus controls measuring ST2 on dried blood spot samples and additionally in pediatric ASD cases versus controls on venous blood together with cardiac magnetic resonance before and after treatment. ST2 was higher in newborns with ASD (

Indexed as

BiomarkersHeart Defects, CongenitalHeart Septal Defects, AtrialInterleukin-1 Receptor-Like 1 ProteinCase-Control StudiesChildChild, PreschoolFemaleHumansInfantInfant, NewbornMaleROC CurveBiomarkersIL1RL1 protein, humanInterleukin-1 Receptor-Like 1 Proteinatrial septal defectcardiac magnetic resonancechildrencongenital heart diseasesoluble growth stimulation protein form of interleukin-1 receptor-like 1ST2

Identifiers

PMID42074089
PMCPMC13115865

What Socratic holds

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Registered trials

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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.