Evidence map›Paper›PMID 42152135›Full record

ArticleStem cell research & therapy2026

Variable cMyBP-C expression from cell to cell in a MYBPC3

Karina Ivaskevica, Kathrin Kowalski, Birgit Piep, Jana Teske, Joachim D Meissner, Maike Kosanke, Ante Radocaj, Judith Montag, Robert Zweigerdt, Theresia Kraft and 1 more

Abstract read
In one paragraph

Article in Stem cell research & therapy, 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

11 authors.

Karina IvaskevicaInstitute of Molecular and Cell Physiology, Hannover Medical School (MHH), Hannover, Germany.
Kathrin KowalskiInstitute of Molecular and Cell Physiology, Hannover Medical School (MHH), Hannover, Germany.
Birgit PiepInstitute of Molecular and Cell Physiology, Hannover Medical School (MHH), Hannover, Germany.
Jana TeskeLeibniz Research Laboratories for Biotechnology and Artificial Organs (LEBAO), Clinic for Cardiac, Thoracic, Transplantation and Vascular Surgery, MHH, Hannover, Germany.
Joachim D MeissnerInstitute of Molecular and Cell Physiology, Hannover Medical School (MHH), Hannover, Germany.
Maike KosankeResearch Core Unit Genomics, Hannover Medical School (MHH), Hannover, Germany.
Ante RadocajInstitute of Molecular and Cell Physiology, Hannover Medical School (MHH), Hannover, Germany.
Judith MontagInstitute of Molecular and Cell Physiology, Hannover Medical School (MHH), Hannover, Germany.
Robert ZweigerdtLeibniz Research Laboratories for Biotechnology and Artificial Organs (LEBAO), Clinic for Cardiac, Thoracic, Transplantation and Vascular Surgery, MHH, Hannover, Germany.
Theresia Kraft *Institute of Molecular and Cell Physiology, Hannover Medical School (MHH), Hannover, Germany.
Sarah A Konze *Institute of Molecular and Cell Physiology, Hannover Medical School (MHH), Hannover, Germany. konze.sarah@mh-hannover.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHypertrophic cardiomyopathy (HCM) is frequently associated with mutations in cardiac myosin binding protein C (cMyBP-C; MYBPC3) and cMyBP-C haploinsufficiency. Previously we discovered burst-like transcription of MYBPC3 and unequal amounts of wild type cMyBP-C from cardiomyocyte to cardiomyocyte in HCM-patient's myocardium. The present study introduces human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) carrying the patient-specific heterozygous MYBPC3 c.927-2 A > G mutation and the respective isogenic control to examine in long-term culture whether comparable pathophysiological features exist in vitro.

methodsWe generated a human induced pluripotent stem cell-derived cardiomyocyte (hiPSC-CM) model harboring the patient-specific MYBPC3 c.927-2 A > G splice-site mutation. An isogenic control line was used for direct comparison. We assessed cMyBP-C protein expression, transcriptional dynamics, contractile function, and calcium handling, and compared the cellular phenotype to heart tissue from the HCM patient with the same mutation.

resultscMyBP-C haploinsufficiency in MYBPC3

conclusionsThis study presents a validated hiPSC-based model of MYBPC3-associated HCM that captures the variability in protein expression and functional phenotype observed in patient heart tissue. Our findings support the relevance of single-cell transcriptional variability in HCM pathogenesis and highlight the utility of this model for future studies.

Indexed as

Cardiomyopathy, HypertrophicCarrier ProteinsInduced Pluripotent Stem CellsMyocytes, CardiacCalciumCell DifferentiationHaploinsufficiencyHumansMutationMyosin Binding Protein CPhenotypeCalciumCarrier ProteinsMyosin Binding Protein CBurst-like transcriptioncMyBP-C expressionDisease modelinghiPSC-derived cardiomyocytesHypertrophic cardiomyopathyMYBPC3 mutation

Identifiers

PMID42152135
PMCPMC13185243

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.