Key result
Deletion of type 2 IP3 receptors did not alter the progression of dilated cardiomyopathy or pressure overload hypertrophy in mouse models, with both strains dying between 10 and 12 weeks of age.
Why the study?
Does deletion of IP3-R(2) prevent disease progression in mouse models of dilated cardiomyopathy or pressure overload hypertrophy?
Population
Mouse models of dilated cardiomyopathy and pressure overload hypertrophy
Comparison
Deletion of type 2 IP3-R (IP3-R(2)-/-) vs Mice with intact IP3-R
Design
Preclinical
Follow-up
up to 10-12 weeks of age
Authors
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IP3-R2 deletion does not modify cardiomyopathy progression in mice; challenges its proposed role and leaves open relevance to human disease.
Does deletion of IP3-R(2) prevent disease progression in mouse models of dilated cardiomyopathy or pressure overload hypertrophy?
Deletion of IP3-R(2) does not contribute to the progression of dilated cardiomyopathy or pressure overload hypertrophy in mouse models.
Cooley et al. (2012) studied Dilated cardiomyopathy and pressure overload hypertrophy. Deletion of type 2 IP3-R (IP3-R(2)-/-) vs. Mice with intact IP3-R(2) was evaluated on Disease progression (chamber dilatation, heart failure, survival). Deletion of type 2 IP3 receptors did not alter the progression of dilated cardiomyopathy or pressure overload hypertrophy in mouse models, with both strains dying between 10 and 12 weeks of age.
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