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Related Concept Videos

Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

65
Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
65

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Patterning Defects in Mice with Defective Ventricular Wall Maturation and Cardiomyopathy.

Javier Santos-Cantador1,2, Marcos Siguero-Álvarez1,2, José Luis de la Pompa1,2

  • 1Intercellular Signaling in Cardiovascular Development and Disease Laboratory, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Calle Melchor Fernández Almagro 3, 28029 Madrid, Spain.

Journal of Cardiovascular Development and Disease
|June 25, 2025
PubMed
Summary
This summary is machine-generated.

Investigating mouse ventricular development reveals distinct gene expression domains, unlike the human heart. Altered spatial gene patterns in a cardiomyopathy model highlight their importance in heart maturation.

Keywords:
LVNCMib1Nrg1cardiac chamber developmentcardiomyopathycellular heterogeneitypatterning

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Area of Science:

  • Cardiovascular Biology
  • Developmental Biology
  • Genetics

Background:

  • Ventricular chamber development requires coordinated cardiomyocyte maturation.
  • Human fetal hearts show regional gene expression differences, while mouse ventricles appear more homogeneous.
  • A transient hybrid cardiomyocyte population exists in mice, expressing both compact and trabecular markers.

Purpose of the Study:

  • To investigate cardiomyocyte marker gene expression in developing mouse ventricles using in situ hybridization (ISH).
  • To compare gene expression patterns between normal and left ventricular non-compaction cardiomyopathy (LVNC) mouse models.
  • To elucidate the role of spatial gene regulation in ventricular development and cardiomyopathy.

Main Methods:

  • In situ hybridization (ISH) was used to examine cardiomyocyte marker gene expression.
  • Analysis was performed on normal and left ventricular non-compaction cardiomyopathy (LVNC) mouse models.
  • Spatial expression patterns of key genes were mapped in developing ventricles.

Main Results:

  • Key marker genes in developing mouse ventricles were restricted to compact and trabecular myocardium domains.
  • Some markers identified non-cardiomyocyte cell types (endocardial, coronary endothelial), differing from human heart patterns.
  • The LVNC model showed altered spatial gene expression, emphasizing the importance of regional organization.

Conclusions:

  • Developing mouse ventricles exhibit a less complex regional gene organization compared to the human fetal heart.
  • Precise spatial gene expression is critical for normal ventricular wall maturation.
  • Spatially regulated gene programs are crucial in ventricular development and may be involved in cardiomyopathy pathogenesis.