Key result
AT(1A) knockout in mice significantly reduced the incidence of apoptosis among granulation tissue cells 1 week post-MI compared to wild-type mice (3.3% vs 4.4%, P<0.05).
Why the study?
Does genetic deletion of the AT(1A) receptor improve infarct scar dynamics and attenuate LV remodeling in a mouse model of myocardial infarction?
Does genetic deletion of the AT(1A) receptor improve infarct scar dynamics and attenuate LV remodeling in a mouse model of myocardial infarction?
Absolute Event Rate: 3.3% vs 4.4%
p-value: p=<0.05
Genetic deletion of the AT1A receptor in mice attenuates post-MI LV remodeling by promoting Akt-mediated cell proliferation and reducing apoptosis in the infarct scar.
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AT1A deletion attenuates murine post-MI apoptosis; hypothesis-generating for remodeling therapies, with no clinical implications yet.
Li et al. (2006) studied Postmyocardial infarction (post-MI) heart failure. ANG II type 1A receptor (AT(1A)) knockout vs. Wild-type (WT) mice was evaluated on Incidence of apoptosis among granulation tissue cells at 1 week post-MI (p=<0.05). AT(1A) knockout in mice significantly reduced the incidence of apoptosis among granulation tissue cells 1 week post-MI compared to wild-type mice (3.3% vs 4.4%, P<0.05).
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