No abstract

Inhibition of AMPK-PGC1a axis impaired mitochondrial biogenesis and was lethal to fatty hepatocyte in vitro, whereas reactivation of AMPK promoted PGC1a-mediated mitochondrial biogenesis and attenuated liver injury via restoring mitochondrial function in animal model. Conclusion:We provided a new mechanism of compromised AMPK-PGC1a axis exacerbated steatotic graft injury in LDLT by driving mitochondrial homeostasis failure through impairment of biogenesis.