Key result
MRTF-A deficiency in mice significantly attenuated hypertrophic responses and BNP gene expression induced by mechanical stress and chronic angiotensin II infusion compared to wild-type mice.
Population
Cardiomyocytes and mice (wild-type and MRTF-A knockout)
Comparison
Mechanical stress and neurohumoral stimulation vs Wild-type mice or unstressed/unstimulated…
Design
Preclinical
Authors
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No immediate clinical implications; leaves open MRTF-A as a therapeutic target in human cardiac hypertrophy.
Nuclear translocation of MRTF-A is a novel signaling mechanism mediating both mechanical stretch- and neurohumoral stimulation-induced BNP gene expression and hypertrophic responses in cardiac myocytes.
Kuwahara et al. (2010) studied Cardiac hypertrophy. MRTF-A deficiency vs. Wild-type was evaluated on Hypertrophic responses and BNP gene expression. MRTF-A deficiency in mice significantly attenuated hypertrophic responses and BNP gene expression induced by mechanical stress and chronic angiotensin II infusion compared to wild-type mice.
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