AMPK: a therapeutic target of heart failure—not only metabolism regulation

Figures

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  Figure 1. Cardiac metabolism in hearts Under normal conditions, cardiomyocytes utilize fatty acids as their major substrate. In the failing heart, the function of mitochondria is impaired. The efficiency of ATP production is dramatically decreased. Cardiomyocytes switch substrate preference to glucose, inducing accumulation of lactate in the failing heart. AMPK regulates multiple related enzymes to promote ATP biosynthesis, ultimately restoring the balance between energy supply and energy demand.

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  Figure 2. AMPK regulates multiple physiological processes to maintain cardiomyocyte homeostasis AMPK activation results in regulation of metabolism, protein transportation, transcription factors, and/or coactivators, kinases, and other enzymes and nonenzymatic proteins. AMPK increases substrate uptake and utilization in cardiomyocytes, enhances mitochondrial biogenesis, and modulates the activity of specific proteins and transcription factors to exert cardioprotective function. Abbreviations: eEF2, eukaryotic elongation factor 2; FAT/CD36, fatty acid translocase; JNK, Jun-amino-terminal kinase; mTOR, mammalian target of rapamycin; ULK1, Unc-51 like kinase 1.