Evidence map›Paper›PMID 42039356›Full record

ArticleFrontiers in cardiovascular medicine2026

Bioenergetic and metabolic aberrations in induced pluripotent stem cell-derived cardiomyocytes generated from a patient with Wolff-Parkinson-White syndrome caused a

Polina Baskin, Ifat Abramovich, Helena Milman, Ronen Ben Jehuda, Bella Agranovich, Mor Davidor, Valerie Buffard, Todd Herron, Ferhaan Ahmad, Michael Arad and 2 more

Abstract read
In one paragraph

Article in Frontiers in cardiovascular medicine, 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

12 authors.

Polina Baskin *Department of Physiology, Biophysics and Systems Biology, Rappaport Faculty of Medicine and Research Institute, Technion, Haifa, Israel.
Ifat Abramovich *Department of Physiology, Biophysics and Systems Biology, Rappaport Faculty of Medicine and Research Institute, Technion, Haifa, Israel.
Helena MilmanDepartment of Physiology, Biophysics and Systems Biology, Rappaport Faculty of Medicine and Research Institute, Technion, Haifa, Israel.
Ronen Ben JehudaDepartment of Physiology, Biophysics and Systems Biology, Rappaport Faculty of Medicine and Research Institute, Technion, Haifa, Israel.
Bella AgranovichPerlmutter Metabolomics Center, Rappaport Faculty of Medicine and Research Institute, Technion, Haifa, Israel.
Mor DavidorDepartment of Physiology, Biophysics and Systems Biology, Rappaport Faculty of Medicine and Research Institute, Technion, Haifa, Israel.
Valerie BuffardDivision of Cardiovascular Medicine, Department of Internal Medicine, University of Iowa, Iowa City, IA, United States.
Todd HerronDepartment of Internal Medicine-Cardiology, University of Michigan, Ann Arbor, MI, United States.
Ferhaan AhmadDivision of Cardiovascular Medicine, Department of Internal Medicine, University of Iowa, Iowa City, IA, United States.
Michael AradHeart Institute, Sheba Medical Center, Faculty of Medicine, Tel-Aviv University, Tel Aviv, Israel.
Melanie Ricke-HochDepartment of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Ofer BinahDepartment of Physiology, Biophysics and Systems Biology, Rappaport Faculty of Medicine and Research Institute, Technion, Haifa, Israel.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: The Methods: Using WPW patient' iPSC-derived cardiomyocytes (iPSC-CMs) and a murine model carrying a Results: We found in mutant iPSC-CMs compared to health iPSC-CMs, reduced glycolytic function and increased maximal mitochondrial respiration associated with elevated mitochondrial content, alongside increased glycogen accumulation, lipid storage and alterations in pathways related to redox regulation. Mutated murine hearts exhibited glycogen accumulation, altered glucose and lipid metabolism, elevated triacylglycerol levels and enhanced fatty acid oxidation pathways. Lipidomic and metabolomic analyses in both models revealed disrupted pathways linked to glucose and lipid metabolism. RNA-seq identified gene expression changes associated with redox regulation, mitochondrial function and hypertrophic signaling, aligned with the observed cellular and tissue-level dysfunction. Metformin treatment reduced mitochondrial content and respiration in mutant iPSC-CMs and significantly attenuated the arrhythmias. Discussion: These findings increase our understanding of

Indexed as

bioenergetic and metabolic profilingcalcium transientsiPSC-derived cardiomyocytes(iPSC-CMs) from a Wolf-Parkinson-White (WPW) patientthe PRKAG2 genetransgenic mice carrying the PRKAG2 thr400Asn (T400N) mutation (TGT400N)Wolf-Parkinson-White syndrome (WPW)

Identifiers

PMID42039356
PMCPMC13106018

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