Key result
Pressure overload fully induced cardiac hypertrophy in AT1A knockout mice similarly to wild-type mice, showing that AT1-mediated Ang II signaling is not essential for its development.
Why the study?
Is AT1-mediated Ang II signaling essential for the development of pressure overload-induced cardiac hypertrophy in mice?
Is AT1-mediated Ang II signaling essential for the development of pressure overload-induced cardiac hypertrophy in mice?
AT1-mediated Ang II signaling is not essential for the development of pressure overload-induced cardiac hypertrophy in a mouse model.
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AT1 signaling dispensable for hypertrophy in mice; leaves open its necessity in human pressure-overload remodeling.
Harada et al. (1998) studied Pressure overload-induced cardiac hypertrophy. AT1A knockout vs. Wild-type mice was evaluated on Cardiac hypertrophy. Pressure overload fully induced cardiac hypertrophy in AT1A knockout mice similarly to wild-type mice, showing that AT1-mediated Ang II signaling is not essential for its development.
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