Key result
Exogenous glucagon administration increased mortality from myocardial infarction in mice, whereas cardiomyocyte-specific inactivation of the glucagon receptor significantly improved survival and reduced infarct size.
Why the study?
Does modulation of glucagon receptor signaling affect infarct size and survival in mice with experimental myocardial infarction?
Population
Normoglycemic non-obese wildtype mice and mice with selective inactivation of the cardiomyocyte glucagon…
Comparison
Exogenous glucagon administration or… vs Wildtype mice with intact glucagon receptor…
Design
Preclinical
Authors
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Reducing cardiomyocyte glucagon signaling improves post-MI survival in mice; leaves open whether antagonism benefits human outcomes.
Does modulation of glucagon receptor signaling affect infarct size and survival in mice with experimental myocardial infarction?
p-value: p=<0.05
Cardiomyocyte-specific reduction of glucagon receptor signaling improves survival and reduces infarct size after myocardial infarction in mice, highlighting potential cardiovascular implications for metabolic therapies targeting this pathway.
Ali et al. (2014) studied Experimental myocardial infarction. Exogenous glucagon or cardiomyocyte-specific Gcgr inactivation vs. Saline or wild-type/aMHCCre littermates was evaluated on Survival following myocardial infarction (p=<0.05). Exogenous glucagon administration increased mortality from myocardial infarction in mice, whereas cardiomyocyte-specific inactivation of the glucagon receptor significantly improved survival and reduced infarct size.
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