Key result
Introduction of CLP-1 haplodeficiency in transgenic α-myosin heavy chain-angiotensinogen mice caused prominent changes in hypertrophic and fibrotic responses and augmented Smad3/Stat3 signaling.
CLP-1 plays a critical role in remodeling the genetic response during cardiac hypertrophy and fibrosis via the Smad3/Stat3 signaling axis.
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Does not inform clinical practice; leaves open CLP-1 as a target in human cardiac remodeling pending translational studies.
Mascareno et al. (2012) studied Left ventricular hypertrophy and fibrosis. CLP-1 haplodeficiency was evaluated on Hypertrophic and fibrotic responses and Smad3/Stat3 signaling. Introduction of CLP-1 haplodeficiency in transgenic α-myosin heavy chain-angiotensinogen mice caused prominent changes in hypertrophic and fibrotic responses and augmented Smad3/Stat3 signaling.
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