ArticleCell reports2015
Contractile Defect Caused by Mutation in MYBPC3 Revealed under Conditions Optimized for Human PSC-Cardiomyocyte Function.
Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
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Who cites it
128 citing papers in PubMed, 1 synthesis or guideline pooled it, 196 citations in OpenAlex.
- Cardiomyopathy phenotypes in human-induced pluripotent stem cell-derived cardiomyocytes-a systematic review.Pflugers Archiv : European journal of physiology · 2019Pooled it
- Recent Developments, Applications, and Future Prospects of Advanced Hearts-on-a-Chip.Micromachines · 2026Review
- Biomechanical stress unmasks a fibroblast-dependent hypercontractile-disarray phenotype in MYBPC3 truncation HCM.APL bioengineering · 2026Article
- Cryopreservation alters contractile function of human induced pluripotent stem cell-derived cardiomyocytes.Scientific reports · 2026Article
- Cross-modal integration of metabolomics and cardiac functionality captures dynamic metabotoxic effects of doxorubicin in engineered heart tissues.Stem cell reports · 2026Article
- Article
- Pluripotent stem cell-based approaches for heart repair and the potential of genetic modifications.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Review
- Metabolic Maturation in hiPSC-Derived Cardiomyocytes: Emerging Strategies for Inducing the Adult Cardiac Phenotype.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Metabolic Culture Medium Enhances Maturation of Human iPSC-Derived Cardiomyocytes via Cardiac Troponin I Isoform Induction.International journal of molecular sciences · 2025Article
- Cardiac differentiation roadmap for analysis of plasticity and balanced lineage commitment.Stem cell reports · 2025Article
- Billion-Scale Expansion of Functional hiPSC-Derived Cardiomyocytes in Bioreactors Through Oxygen Control and Continuous Wnt Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Revitalizing the heart: strategies and tools for cardiomyocyte regeneration post-myocardial infarction.NPJ Regenerative medicine · 2025Review
- FORCETRACKER: A versatile tool for standardized assessment of tissue contractile properties in 3D Heart-on-Chip platforms.PloS one · 2025Article
- Article
- Article
- Independent compartmentalization of functional, metabolic, and transcriptional maturation of hiPSC-derived cardiomyocytes.Cell reports · 2024Article
- Myosin inhibitor reverses hypertrophic cardiomyopathy in genotypically diverse pediatric iPSC-cardiomyocytes to mirror variant correction.Cell reports. Medicine · 2024Article
- Article
- The past, present, and future promise of pluripotent stem cells.Journal of immunology and regenerative medicine · 2024Article
68 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Maximizing baseline function of human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) is essential for their effective application in models of cardiac toxicity and disease. Here, we aimed to identify factors that would promote an adequate level of function to permit robust single-cell contractility measurements in a human induced pluripotent stem cell (hiPSC) model of hypertrophic cardiomyopathy (HCM). A simple screen revealed the collaborative effects of thyroid hormone, IGF-1 and the glucocorticoid analog dexamethasone on the electrophysiology, bioenergetics, and contractile force generation of hPSC-CMs. In this optimized condition, hiPSC-CMs with mutations in MYBPC3, a gene encoding myosin-binding protein C, which, when mutated, causes HCM, showed significantly lower contractile force generation than controls. This was recapitulated by direct knockdown of MYBPC3 in control hPSC-CMs, supporting a mechanism of haploinsufficiency. Modeling this disease in vitro using human cells is an important step toward identifying therapeutic interventions for HCM.
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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 OpenQuestion graph.