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• W1994566639 abstract "A specific role for Akt1 in events following myocardial infarction (MI) and ischemia/reperfusion (I/R) injury is not known. We aimed to determine whether Akt1 deletion in in vivo mouse models of MI and after ischemia I/R injury would alter myocyte survival, cardiac function, and fibrosis. Akt1+/+ and Akt1−/− mice were subjected to MI and I/R, followed by assessment of downstream signaling events and functional consequences. Although no difference in infarct size following short-term MI was observed between Akt1+/+ and Akt1−/− mice, I/R caused substantially more cardiomyocyte apoptosis and tissue damage in Akt1−/− mice compared with Akt1+/+. Importantly, these effects were reversed upon pretreatment with GSK-3 inhibitor SB415286. Counterintuitively, Akt1−/− hearts exhibited improved cardiac function following long-term MI compared with Akt1+/+ and were associated with reduced fibrosis in the left ventricle (LV). Our results demonstrate that Akt1-mediated inhibition of GSK-3 activity is critical for cardioprotection following I/R. However, in the long term, Akt1 contributes to fibrosis in post-MI hearts and might exacerbate cardiac dysfunction showing dichotomous role for Akt1 in cardiac remodeling after MI. Our data suggest that better understanding of the Akt1/GSK-3 pathway may provide insights for better therapeutic strategies in post-MI tissues." @default.
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• W1994566639 date "2014-10-01" @default.
• W1994566639 modified "2023-10-07" @default.
• W1994566639 title "Differential effects of Akt1 signaling on short- versus long-term consequences of myocardial infarction and reperfusion injury" @default.
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• W1994566639 doi "https://doi.org/10.1038/labinvest.2014.95" @default.
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