Guanylyl Cyclase-A Inhibits Angiotensin II Type 1A Receptor-Mediated Cardiac Remodeling, an Endogenous Protective Mechanism in the Heart
Population
GC-A-deficient mice
Design
Preclinical
Authors
Discussion
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Member takes
Implication
Should not change clinical practice; hypothesis-generating for GC-A-AT1A interactions in human remodeling.
Structured PICO
P
Population
GC-A-deficient mice
O
Outcome
Cardiac hypertrophy and fibrosissurrogate
Guanylyl Cyclase-A acts as an endogenous protective mechanism against cardiac remodeling by inhibiting AT1A receptor-mediated signaling.
Cite This Study
Li et al. (2002) studied this question.