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Abnormal ventricular wall patterning precedes and drives MYBPC3 hypertrophic cardiomyopathy

https://doi.org/10.64898/2026.03.25.714341

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Outgoing claims: the papers this work cites, builds on, or argues with.

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The Burden of Early Phenotypes and the Influence of Wall Thickness in Hypertrophic Cardiomyopathy Mutation Carriers

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Cardiomyopathy due to PRDM16 mutation: First description of a fetal presentation, with possible modifier genes

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A global double‐fluorescent Cre reporter mouse

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Rapid Transition of Cardiac Myocytes from Hyperplasia to Hypertrophy During Postnatal Development

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The Role of TGF—β Signaling in Cardiomyocyte Proliferation

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Fine Mapping of the 1p36 Deletion Syndrome Identifies Mutation of PRDM16 as a Cause of Cardiomyopathy

inferredcites →https://doi.org/10.1016/j.cardiores.2004.04.009openalex-snapshot

Asymmetric septal hypertrophy in heterozygous cMyBP-C null mice

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Advances in the study and treatment of genetic cardiomyopathies

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Prdm16 Deficiency Leads to Age-Dependent Cardiac Hypertrophy, Adverse Remodeling, Mitochondrial Dysfunction, and Heart Failure

inferredcites →https://doi.org/10.1016/j.cmet.2019.05.005openalex-snapshot

A PRDM16-Driven Metabolic Signal from Adipocytes Regulates Precursor Cell Fate

inferredcites →https://doi.org/10.1016/j.jacc.2014.10.069openalex-snapshot

Irreversible Triggers for Hypertrophic Cardiomyopathy Are Established in the Early Postnatal Period

inferredcites →https://doi.org/10.1016/j.jacc.2017.12.019openalex-snapshot

Genetics, Clinical Features, and Long-Term Outcome of Noncompaction Cardiomyopathy

inferredcites →https://doi.org/10.1016/j.jmccpl.2025.100517openalex-snapshot

Broad therapeutic benefit of myosin inhibition in hypertrophic cardiomyopathy

inferredcites →https://doi.org/10.1016/s0140-6736(14)61282-4openalex-snapshot

Left ventricular non-compaction cardiomyopathy

inferredcites →https://doi.org/10.1038/ncb3280openalex-snapshot

Sequential Notch activation regulates ventricular chamber development

inferredcites →https://doi.org/10.1038/ncb3411openalex-snapshot

iPSC-derived cardiomyocytes reveal abnormal TGF-β signalling in left ventricular non-compaction cardiomyopathy

inferredcites →https://doi.org/10.1038/nm.3046openalex-snapshot

Mutations in the NOTCH pathway regulator MIB1 cause left ventricular noncompaction cardiomyopathy

inferredcites →https://doi.org/10.1038/s41436-020-01049-xopenalex-snapshot

Systematic large-scale assessment of the genetic architecture of left ventricular noncompaction reveals diverse etiologies

inferredcites →https://doi.org/10.1038/s41467-017-00118-1openalex-snapshot

Identification of a hybrid myocardial zone in the mammalian heart after birth

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Minor hypertrophic cardiomyopathy genes, major insights into the genetics of cardiomyopathies

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The embryological basis of subclinical hypertrophic cardiomyopathy

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Myocardial Fibrosis as an Early Manifestation of Hypertrophic Cardiomyopathy

inferredcites →https://doi.org/10.1056/nejmra0902923openalex-snapshot

Inherited Cardiomyopathies

inferredcites →https://doi.org/10.1073/pnas.1511004112openalex-snapshot

Cardiac myosin binding protein C regulates postnatal myocyte cytokinesis

inferredcites →https://doi.org/10.1074/jbc.m110.156646openalex-snapshot

Structure and Interactions of Myosin-binding Protein C Domain C0

inferredcites →https://doi.org/10.1085/jgp.202213204openalex-snapshot

cMyBP-C ablation in human engineered cardiac tissue causes progressive Ca2+-handling abnormalities

inferredcites →https://doi.org/10.1085/jgp.202213318openalex-snapshot

The contribution of N-terminal truncated cMyBPC to in vivo cardiac function

inferredcites →https://doi.org/10.1093/cvr/cvaa159openalex-snapshot

The long and winding road of cardiomyocyte maturation

inferredcites →https://doi.org/10.1096/fasebj.5.15.1835945openalex-snapshot

Regulation of cardiac gene expression during myocardial growth and hypertrophy: molecular studies of an adaptive physiologic response

inferredcites →https://doi.org/10.1101/cshperspect.a023200openalex-snapshot

Muscle Contraction

inferredcites →https://doi.org/10.1101/gad.1124803openalex-snapshot

An essential role of Bmp4 in the atrioventricular septation of the mouse heart

inferredcites →https://doi.org/10.1111/j.1469-7793.2000.00151.xopenalex-snapshot

A role for C‐protein in the regulation of contraction and intracellular Ca2+ in intact rat ventricular myocytes

inferredcites →https://doi.org/10.1136/hrt.2005.082271openalex-snapshot

Isolated ventricular non-compaction of the myocardium in adults

inferredcites →https://doi.org/10.1136/jmg-2025-110696openalex-snapshot

Contemporary practice and resource availability for genetic testing in paediatric hypertrophic cardiomyopathy

inferredcites →https://doi.org/10.1161/01.cir.101.12.1396openalex-snapshot

A Newly Created Splice Donor Site in Exon 25 of the MyBP-C Gene Is Responsible for Inherited Hypertrophic Cardiomyopathy With Incomplete Disease Penetrance

inferredcites →https://doi.org/10.1161/01.res.0000012222.70819.64openalex-snapshot

Hypertrophic Cardiomyopathy in Cardiac Myosin Binding Protein-C Knockout Mice

inferredcites →https://doi.org/10.1161/01.res.85.9.841openalex-snapshot

In Vivo Modeling of Myosin Binding Protein C Familial Hypertrophic Cardiomyopathy

inferredcites →https://doi.org/10.1161/circgen.120.002929openalex-snapshot

Spatial and Functional Distribution of MYBPC3 Pathogenic Variants and Clinical Outcomes in Patients With Hypertrophic Cardiomyopathy

inferredcites →https://doi.org/10.1161/circgenetics.109.903898openalex-snapshot

The Importance of Genetic Counseling, DNA Diagnostics, and Cardiologic Family Screening in Left Ventricular Noncompaction Cardiomyopathy

inferredcites →https://doi.org/10.1161/circgenetics.113.000362openalex-snapshot

Abnormal Cardiac Formation in Hypertrophic Cardiomyopathy

inferredcites →https://doi.org/10.1161/circheartfailure.117.004140openalex-snapshot

Activation of Autophagy Ameliorates Cardiomyopathy in Mybpc3 -Targeted Knockin Mice

inferredcites →https://doi.org/10.1161/circheartfailure.122.010351openalex-snapshot

Nonsense Variant PRDM16-Q187X Causes Impaired Myocardial Development and TGF-β Signaling Resulting in Noncompaction Cardiomyopathy in Humans and Mice

inferredcites →https://doi.org/10.1161/circresaha.109.201251openalex-snapshot

Nonsense-Mediated mRNA Decay and Ubiquitin–Proteasome System Regulate Cardiac Myosin-Binding Protein C Mutant Levels in Cardiomyopathic Mice

inferredcites →https://doi.org/10.1161/circresaha.109.202440openalex-snapshot

Evidence From Human Myectomy Samples That MYBPC3 Mutations Cause Hypertrophic Cardiomyopathy Through Haploinsufficiency

inferredcites →https://doi.org/10.1161/circresaha.117.311059openalex-snapshot

Hypertrophic Cardiomyopathy

inferredcites →https://doi.org/10.1161/circresaha.119.315862openalex-snapshot

Cardiomyocyte Maturation

inferredcites →https://doi.org/10.1161/circulationaha.108.838672openalex-snapshot

Cardiac Myosin-Binding Protein C Mutations and Hypertrophic Cardiomyopathy

inferredcites →https://doi.org/10.1161/circulationaha.111.089219openalex-snapshot

Dissociation of Structural and Functional Phenotypes in Cardiac Myosin-Binding Protein C Conditional Knockout Mice

inferredcites →https://doi.org/10.1161/circulationaha.118.034624openalex-snapshot

A Premature Termination Codon Mutation in MYBPC3 Causes Hypertrophic Cardiomyopathy via Chronic Activation of Nonsense-Mediated Decay

inferredcites →https://doi.org/10.1161/circulationaha.121.056666openalex-snapshot

PRDM16 Is a Compact Myocardium-Enriched Transcription Factor Required to Maintain Compact Myocardial Cardiomyocyte Identity in Left Ventricle

inferredcites →https://doi.org/10.1161/circulationaha.121.058767openalex-snapshot

A Human Hereditary Cardiomyopathy Shares a Genetic Substrate With Bicuspid Aortic Valve

inferredcites →https://doi.org/10.1161/hh1301.092687openalex-snapshot

Temporally Regulated and Tissue-Specific Gene Manipulations in the Adult and Embryonic Heart Using a Tamoxifen-Inducible Cre Protein

inferredcites →https://doi.org/10.1161/jaha.115.002836openalex-snapshot

Alterations in Multi‐Scale Cardiac Architecture in Association With Phosphorylation of Myosin Binding Protein‐C

inferredcites →https://doi.org/10.1172/jci.insight.133782openalex-snapshot

Effects of MYBPC3 loss-of-function mutations preceding hypertrophic cardiomyopathy

inferredcites →https://doi.org/10.1172/jci119555openalex-snapshot

Novel splice donor site mutation in the cardiac myosin-binding protein-C gene in familial hypertrophic cardiomyopathy. Characterization Of cardiac transcript and protein.

inferredcites →https://doi.org/10.1186/s13023-021-02112-9openalex-snapshot

Overlap phenotypes of the left ventricular noncompaction and hypertrophic cardiomyopathy with complex arrhythmias and heart failure induced by the novel truncated DSC2 mutation

inferredcites →https://doi.org/10.1242/dev.119.2.485openalex-snapshot

Defects in heart and lung development in compound heterozygotes for two different targeted mutations at the N-myc locus

inferredcites →https://doi.org/10.1371/journal.pone.0217612openalex-snapshot

Defining genotype-phenotype relationships in patients with hypertrophic cardiomyopathy using cardiovascular magnetic resonance imaging

inferredcites →https://doi.org/10.1371/journal.pone.0267938openalex-snapshot

A cardiac-null mutation of Prdm16 causes hypotension in mice with cardiac hypertrophy via increased nitric oxide synthase 1

inferredcites →https://doi.org/10.2174/1566523218666180709125346openalex-snapshot

Phenotypic Characterization of a Family With An In-frame Deletion in the DMD Gene and Variable Penetrance

inferredcites →https://doi.org/10.26508/lsa.202402719openalex-snapshot

PRDM16 determines specification of ventricular cardiomyocytes by suppressing alternative cell fates

inferredcites →https://doi.org/10.3389/fphys.2018.01442openalex-snapshot

Transcriptome Analysis of Cardiac Hypertrophic Growth in MYBPC3-Null Mice Suggests Early Responders in Hypertrophic Remodeling

inferredcites →https://doi.org/10.3390/jcm9103171openalex-snapshot

Trabeculated Myocardium in Hypertrophic Cardiomyopathy: Clinical Consequences

inferredcites →https://doi.org/10.4330/wjc.v16.i9.496openalex-snapshot

Hypertrophic cardiomyopathy and left ventricular non-compaction: Distinct diseases or variant phenotypes of a single condition?

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