Key result
Genetically engineered mouse models demonstrate that disruptions in Notch, BMP10, and noncanonical Wnt/PCP signaling pathways contribute to the pathogenesis of left ventricular noncompaction.
Population
Genetically engineered mouse models with defects in cardiac trabeculation and compaction
Design
Review
Authors
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Mouse models of LVNC pathways require human validation; leaves open therapeutic targeting of Notch, BMP10, or Wnt/PCP.
This review highlights the critical roles of BMP10, Notch, and Wnt/PCP signaling pathways in ventricular wall development, providing molecular insights into the pathogenesis of left ventricular noncompaction cardiomyopathy.
Zhang et al. (2013) conducted a review in Left ventricular noncompaction cardiomyopathy (LVNC). Genetically engineered mouse models demonstrate that disruptions in Notch, BMP10, and noncanonical Wnt/PCP signaling pathways contribute to the pathogenesis of left ventricular noncompaction.
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