ArticleJournal of molecular and cellular cardiology2016
Deficient cMyBP-C protein expression during cardiomyocyte differentiation underlies human hypertrophic cardiomyopathy cellular phenotypes in disease specific human ES cell derived cardiomyocytes.
Article in Journal of molecular and cellular cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 49 citations in OpenAlex.
- Variable cMyBP-C expression from cell to cell in a MYBPC3Stem cell research & therapy · 2026Article
- A New Era in the Management of Hypertrophic Cardiomyopathy.Reviews in cardiovascular medicine · 2025Review
- Current and emerging medical and surgical therapy in hypertrophic cardiomyopathy.Journal of cardiovascular imaging · 2025Review
- Experimental Models of Hypertrophic Cardiomyopathy: A Systematic Review.JACC. Basic to translational science · 2025Review
- Unveiling the Future of Cardiac Care: A Review of Gene Therapy in Cardiomyopathies.International journal of molecular sciences · 2024Review
- An Unbiased Screen Identified the Hsp70-BAG3 Complex as a Regulator of Myosin-Binding Protein C3.JACC. Basic to translational science · 2023Article
- High-throughput longitudinal electrophysiology screening of mature chamber-specific hiPSC-CMs using optical mapping.iScience · 2023Article
- An Update on MYBPC3 Gene Mutation in Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2023Review
- A Narrative Review of Emerging Therapies for Hypertrophic Obstructive Cardiomyopathy.Current cardiology reviews · 2023Review
- Familial Hypertrophic Cardiomyopathy: Diagnosis and Management.Vascular health and risk management · 2023Review
- Molecular Diagnosis of Hypertrophic Cardiomyopathy (HCM): In the Heart of Cardiac Disease.Journal of clinical medicine · 2022Review
- Contemporary Therapies and Future Directions in the Management of Hypertrophic Cardiomyopathy.Cardiology and therapy · 2022Review
- Brugada Syndrome: Different Experimental Models and the Role of Human Cardiomyocytes From Induced Pluripotent Stem Cells.Journal of the American Heart Association · 2022Review
- Calcium handling maturation and adaptation to increased substrate stiffness in human iPSC-derived cardiomyocytes: The impact of full-length dystrophin deficiency.Frontiers in physiology · 2022Article
- In vitro model of ischemic heart failure using human induced pluripotent stem cell-derived cardiomyocytes.JCI insight · 2021Article
- Genetic Cardiomyopathies: The Lesson Learned from hiPSCs.Journal of clinical medicine · 2021Review
- Hypertrophic Cardiomyopathy: From Phenotype and Pathogenesis to Treatment.Frontiers in cardiovascular medicine · 2021Review
- Non-pharmaceutical Interventions for Hypertrophic Cardiomyopathy: A Mini Review.Frontiers in cardiovascular medicine · 2021Review
- Optimizing the Use of iPSC-CMs for Cardiac Regeneration in Animal Models.Animals : an open access journal from MDPI · 2020Review
- Developmental potential of aneuploid human embryos cultured beyond implantation.Nature communications · 2020Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
aimsMutations of cardiac sarcomere genes have been identified to cause HCM, but the molecular mechanisms that lead to cardiomyocyte hypertrophy and risk for sudden death are uncertain. The aim of this study was to examine HCM disease mechanisms at play during cardiac differentiation of human HCM specific pluripotent stem cells. METHODS AND
resultsWe generated a human embryonic stem cell (hESC) line carrying a naturally occurring mutation of MYPBC3 (c.2905 +1 G >A) to study HCM pathogenesis during cardiac differentiation. HCM-specific hESC-derived cardiomyocytes (hESC-CMs) displayed hallmark aspects of HCM including sarcomere disarray, hypertrophy and impaired calcium impulse propagation. HCM hESC-CMs presented a transient haploinsufficiency of cMyBP-C during cardiomyocyte differentiation, but by day 30 post-differentiation cMyBP-C levels were similar to control hESC-CMs. Gene transfer of full-length MYBPC3 during differentiation prevented hypertrophy, sarcomere disarray and improved calcium impulse propagation in HCM hESC-CMs. CONCLUSION(S): These findings point to the critical role of MYBPC3 during sarcomere assembly in cardiac myocyte differentiation and suggest developmental influences of MYBPC3 truncating mutations on the mature hypertrophic phenotype.
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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.