Key result
Cardiac M21 overexpression induces histological myocyte hypertrophy in mice without altering overall cardiac function.
Why the study?
Does overexpression of the human M21 subunit of MLCP induce cardiac hypertrophy or alter cardiac function in mice?
Population
Transgenic mice overexpressing the human heart-specific small-subunit of myosin light chain phosphatase…
Comparison
Overexpression of human M21 and chronic cardiac… vs Non-transgenic littermates
Design
Preclinical
Follow-up
Up to 3 months of age; 2 weeks for isoproterenol stress
Authors
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Does not alter murine cardiac function despite histological hypertrophy; leaves open translational relevance to human remodeling.
Does overexpression of the human M21 subunit of MLCP induce cardiac hypertrophy or alter cardiac function in mice?
Overexpression of the human M21 subunit of MLCP in murine hearts induces histological myocyte hypertrophy without affecting overall cardiac function under normal or stressed conditions.
Bae et al. (2003) studied Cardiac hypertrophy. Overexpression of human M21 (small-subunit of MLCP) vs. Non-transgenic littermates was evaluated on Echocardiographic determinants (left ventricular dimensions and wall thickness) and histological morphology. Overexpression of the human M21 small-subunit of MLCP in the murine heart induced myocyte hypertrophy histologically, but did not significantly affect overall cardiac function or echocardiographic parameters.
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