Key result
Cardiac-specific deletion of PKD1 in mice diminished cardiac hypertrophy, resulting in only a 23% increase in heart weight/tibia length ratio compared to a 47% increase in wild-type mice after pressure overload.
Why the study?
Does cardiac-specific deletion of PKD1 prevent pathological cardiac remodeling in response to stress stimuli in mice?
Population
Mice with a conditional PKD1-null allele subjected to pressure overload or chronic adrenergic and…
Design
Preclinical
Authors
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PKD1 deletion attenuates stress-induced hypertrophy in mice; leaves open its therapeutic targeting in human heart failure.
Does cardiac-specific deletion of PKD1 prevent pathological cardiac remodeling in response to stress stimuli in mice?
Absolute Event Rate: 23% vs 47%
PKD1 functions as a key transducer of stress stimuli involved in pathological cardiac remodeling in vivo, highlighting its potential role in heart failure pathogenesis.
Fielitz et al. (2008) studied Pathological cardiac remodeling. Cardiac-specific deletion of PKD1 vs. Wild-type littermates was evaluated on Increase in heart weight/tibia length (HW/TL) ratio after thoracic aortic constriction. Cardiac-specific deletion of PKD1 in mice diminished cardiac hypertrophy, resulting in only a 23% increase in heart weight/tibia length ratio compared to a 47% increase in wild-type mice after pressure overload.
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