Key result
Induction of ssARKct expression via the CARP promoter during pressure overload preserved myocardial ssAR responsiveness and inotropic reserve in vivo compared to nontransgenic littermates.
Why the study?
Does physiological induction of a ssARKct transgene preserve ss-adrenergic responsiveness in mice with pressure-overload cardiac hypertrophy?
Population
Transgenic mice with myocardium-targeted ssARKct transgene expression under control of the CARP promoter…
Comparison
Transverse aortic constriction to induce… vs Nontransgenic littermates (NLCs) subjected to TAC
Design
Preclinical
Follow-up
7 days
Authors
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May inform βARKct-targeted therapies in heart failure; leaves open translation from rodent models to clinical practice.
Does physiological induction of a ssARKct transgene preserve ss-adrenergic responsiveness in mice with pressure-overload cardiac hypertrophy?
Physiological induction of a ssARKct transgene using the CARP promoter preserves ss-adrenergic responsiveness and inotropic reserve in a mouse model of pressure-overload cardiac hypertrophy.
Manning et al. (2000) studied Pressure-overload cardiac hypertrophy. Induced ssARKct expression (via CARP promoter) vs. Nontransgenic littermates (NLCs) was evaluated on ssAR responsiveness and inotropic reserve. Induction of ssARKct expression via the CARP promoter during pressure overload preserved myocardial ssAR responsiveness and inotropic reserve in vivo compared to nontransgenic littermates.
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