Key result
Notch blockade in newborn mice causes dilated myopathy and high mortality, driven by ~54% fewer myocytes.
Why the study?
Does Notch pathway blockade induce dilated myopathy and impair cardiomyogenesis in newborn mice?
Population
Newborn mice and neonatal cardiac stem cells (CSCs)
Design
Preclinical
Authors
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Notch modulation may risk neonatal cardiomyogenesis; hypothesis-generating for human congenital dilated myopathy.
Does Notch pathway blockade induce dilated myopathy and impair cardiomyogenesis in newborn mice?
Notch1 signaling is essential for neonatal cardiomyogenesis, and its inhibition leads to impaired physiological hypertrophy and a life-threatening dilated myopathy.
Urbanek et al. (2010) studied Neonatal heart development. Gamma-secretase inhibitor (Notch pathway blockade) was evaluated on Myocyte number and ventricular decompensation. Blockade of the Notch pathway in newborn mice resulted in a 62% reduction in amplifying myocytes and a 54% decrease in myocyte number, leading to a dilated myopathy and high mortality.
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