HIF-1/AKT Signaling-Activated PFKFB2 Alleviates Cardiac Dysfunction and Cardiomyocyte Apoptosis in Response to Hypoxia

Myocardial infarction (MI) is the most prevalent disease with severe mortality, and hypoxia-induced cardiac injury cardiomyocyte apoptosis are significant harmful consequences of this disease. The cross talk between hypoxia signaling glycolysis energy flux plays a critical role in modulating MI-related heart disorder. However, underlying mechanism remains unclear. Here, we aimed to explore effect key glycolytic enzyme 6-phosphofructo-2-kinase/fructose-2, 6-bisphosphatase 2 (PFKFB2) on dysfunction response hypoxia. Our data demonstrated that mRNA protein expression PFKFB2 were significantly elevated MI mice. treatment promoted activation vivo, as presented by remarkably increased phosphorylation levels PFKFB2. depletion enhanced MI-induced mouse model. Moreover, dramatically upregulated time-dependent manner cardiomyocytes. Hypoxia-stimulated relieved vitro. activated fructose-2, 6-bisphosphate (Fru-2, 6-p2) /PFK/anaerobic adenosine triphosphate (ATP) Mechanically, hypoxia-activated stimulating hypoxia-inducible factor 1 (HIF-1) /ATK signaling. Thus, conclude HIF-1/AKT axis-activated alleviates finding presents new insight into which HIF-1/AKT/PFKFB2 modulates disorder under condition, providing potential therapeutic targets strategy for hypoxia-related myocardial injury.