Journal
PEDIATRIC CARDIOLOGY
Volume 30, Issue 5, Pages 626-634Publisher
SPRINGER
DOI: 10.1007/s00246-009-9406-5
Keywords
Ventricular development; Trabeculation and compaction; Signaling
Categories
Funding
- NHLBI NIH HHS [R01 HL070259, P01 HL085098-01A10003, HL70259, R01 HL081092, HL81092, P01 HL085098, HL85098] Funding Source: Medline
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Ventricular trabeculation and compaction are two of the many essential steps for generating a functionally competent ventricular wall. A significant reduction in trabeculation is usually associated with ventricular compact zone deficiencies (hypoplastic wall), which commonly lead to embryonic heart failure and early embryonic lethality. In contrast, hypertrabeculation and lack of ventricular wall compaction (noncompaction) are closely related defects in cardiac embryogenesis associated with left ventricular noncompaction, a genetically heterogeneous disorder. Here we summarize our recent findings through the analyses of several genetically engineered mouse models that have defects in cardiac trabeculation and compaction. Our data indicate that cellular growth and differentiation signaling pathways are keys in these ventricular morphogenetic events.
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