Evidence map›Paper›PMID 41707622›Full record

ArticleJACC. Basic to translational science2026

Abnormal Lipid Signaling Characterizes Diastolic Dysfunction in Pediatric Cardiomyopathy.

Andrei L Turinsky, Nour Hanafi, Abdelrahman Said, Caroline Kinnear, Robert Lesurf, José Luis López-Guillén, Rajadurai Akilen, Suhani Patel, Guoliang Meng, Wei Wei and 6 more

Abstract read
In one paragraph

Article in JACC. Basic to translational science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
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

16 authors.

Andrei L TurinskyCentre for Computational Medicine, Hospital for Sick Children, Toronto, Ontario, Canada.
Nour HanafiCentre for Computational Medicine, Hospital for Sick Children, Toronto, Ontario, Canada.
Abdelrahman SaidGenetics and Genome Biology Program, Hospital for Sick Children, Toronto, Ontario, Canada.
Caroline KinnearGenetics and Genome Biology Program, Hospital for Sick Children, Toronto, Ontario, Canada.
Robert LesurfGenetics and Genome Biology Program, Hospital for Sick Children, Toronto, Ontario, Canada.
José Luis López-GuillénDepartment of Pediatrics, Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada.
Rajadurai AkilenGenetics and Genome Biology Program, Hospital for Sick Children, Toronto, Ontario, Canada.
Suhani PatelGenetics and Genome Biology Program, Hospital for Sick Children, Toronto, Ontario, Canada.
Guoliang MengDevelopmental and Stem Cell Biology Program, Hospital for Sick Children, Toronto, Ontario, Canada.
Wei WeiDevelopmental and Stem Cell Biology Program, Hospital for Sick Children, Toronto, Ontario, Canada.
Isabelle Robillard FrayneMontreal Heart Institute, Metabolomics platform, Montreal, Quebec, Canada.
Caroline DaneaultMontreal Heart Institute, Metabolomics platform, Montreal, Quebec, Canada; Department of Nutrition, Université de Montréal, Montréal, Quebec, Canada.
Luc MertensDepartment of Pediatrics, Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada.
James EllisDevelopmental and Stem Cell Biology Program, Hospital for Sick Children, Toronto, Ontario, Canada; Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada.
Matthieu RuizMontreal Heart Institute, Metabolomics platform, Montreal, Quebec, Canada; Department of Nutrition, Université de Montréal, Montréal, Quebec, Canada.
Seema MitalGenetics and Genome Biology Program, Hospital for Sick Children, Toronto, Ontario, Canada; Department of Pediatrics, Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada; Ted Rogers Centre for Heart Research, Toronto, Ontario, Canada. Electronic address: seema.mital@sickkids.ca.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pediatric cardiomyopathy is a major cause of diastolic heart failure; yet, its mechanisms remain unclear. Global myocardial transcriptomic and blood lipidomic profiling revealed a distinct metabolic signature of diastolic dysfunction marked by dysregulated lipid signaling. A machine learning model using these gene markers accurately classified diastolic dysfunction across cardiomyopathy subtypes. Lipidomic changes included excess saturated lipids and impaired oxidation that correlated with myocardial gene expression. Induced pluripotent stem cell cardiomyocytes from patients with diastolic dysfunction exhibited lipid accumulation, and mitochondrial dysfunction that was rescued by semaglutide. These findings define a new molecular phenotype of diastolic dysfunction and point to abnormal lipid signaling as a promising therapeutic target in childhood cardiomyopathy.

Indexed as

cardiomyopathydiastolic dysfunctioniPSC cardiomyocyteslipidomemultiomicsRNA sequencing

Identifiers

PMID41707622
PMCPMC12926570

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.