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• W1534476908 abstract "Summary. Background: Modulation of energy substrate metabolism may constitute a novel therapeutic intervention against ischemia/reperfusion (I/R) injury. AMP-activated protein kinase (AMPK) has emerged as a key regulator of favorable metabolic signaling pathways in response to myocardial ischemia. Recently, we demonstrated that activated protein C (APC) is cardioprotective against ischemia/reperfusion (I/R) injury by augmenting AMPK signaling. Objectives: The objective of this study was to determine whether the APC modulation of substrate metabolism contributes to its cardioprotective effect against I/R injury. Methods: An ex vivo working mouse heart perfusion system was used to characterize the effect of wild-type APC and its signaling-proficient mutant, APC-2Cys (which has dramatically reduced anticoagulant activity), on glucose transport in the ischemic heart. Results: Both APC and APC-2Cys (0.2 μg g−1) augment the ischemic stress-induced translocation of the glucose transporter (GLUT4) to the myocardial cell membrane, leading to increased glucose uptake and glucose oxidation in the ischemic heart (P < 0.05 vs. vehicle). Both APC derivatives increased the autophagic flux in the heart following I/R. The activity of APC-2Cys in modulating these metabolic pathways was significantly higher than APC during I/R (P < 0.05). Intriguingly, APC-2Cys, but not wild-type APC, attenuated the I/R-initiated fatty acid oxidation by 80% (P < 0.01 vs. vehicle). Conclusions: APC exerts a cardioprotective effect against I/R injury by preferentially enhancing the oxidation of glucose over fatty acids as energy substrates in the ischemic heart. Given its significantly higher beneficial metabolic modulatory effect, APC-2Cys may be developed as a potential therapeutic drug for treating ischemic heart disease without risk of bleeding." @default.
• W1534476908 created "2016-06-24" @default.
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• W1534476908 date "2012-09-01" @default.
• W1534476908 modified "2023-10-15" @default.
• W1534476908 title "Activated protein C modulates cardiac metabolism and augments autophagy in the ischemic heart" @default.
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• W1534476908 doi "https://doi.org/10.1111/j.1538-7836.2012.04833.x" @default.
• W1534476908 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3433592" @default.
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