Why the study?
Does the absence of the PKA Cβ subunit protect mice from angiotensin II-induced cardiac hypertrophy and dysfunction?
Population
Mice subjected to angiotensin II-induced hypertension
Comparison
Genetic deletion of the catalytic β subunit of PKA vs Wild-type (WT) littermates
Design
Preclinical
Authors
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PKA Cβ may represent a therapeutic target in hypertrophy; hypothesis-generating in mice and leaves open human translation.
Does the absence of the PKA Cβ subunit protect mice from angiotensin II-induced cardiac hypertrophy and dysfunction?
The Cβ subunit of PKA plays a critical role in angiotensin-induced cardiac dysfunction, highlighting its potential as a pharmaceutical target for hypertrophic cardiac disease.
Enns et al. (2010) studied this question.
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