Muscle LIM protein (MLP) has been proposed to be a central player in the 
pathogenesis of heart muscle disease. In line with this notion, the homozygous 
loss of MLP results in cardiac hypertrophy and dilated cardiomyopathy. Moreover, 
MLP is induced in several models of cardiac hypertrophy such as aortic banding 
and myocardial infarction. We thus hypothesized that overexpression of MLP might 
change the hypertrophic response to cardiac stress. In order to answer the 
question whether MLP modulates cardiac hypertrophy in vivo, we generated a novel 
transgenic mouse model with cardiac-specific overexpression of MLP. Three 
independent transgenic lines did not show a pathological phenotype under 
baseline conditions. Specifically, contractile function and heart weight to body 
weight ratios at different ages were normal. Next, the transgenic animals were 
challenged with pressure overload due to aortic constriction. Surprisingly, 
transgenic mice developed cardiac hypertrophy to the same extent as their 
wild-type littermates. Moreover, neither contractile dysfunction nor 
pathological gene expression in response to pressure overload were 
differentially affected by MLP overexpression. Finally, in a milder in vivo 
model of hypertrophy induced by chronic infusion of angiotensin-II, cardiac mass 
and hypertrophic gene expression were again identical in MLP transgenic mice and 
controls. Taken together, we provide evidence that cardiac overexpression of MLP 
does not modulate the heart's response to various forms of pathological stress.