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A proposed overview of AMPK-dependent regulation of sepsis-induced liver injury in young and mature mice. During sepsis, AMPK is activated in the nucleus in young mice as a compensatory mechanism to maintain energy homeostasis and limit mitochondrial damage by increased autophagy. On the contrary, nuclear down-regulation of AMPK in mature mice is associated with energy failure and extensive mitochondrial damage with impaired autophagy resulting in severe liver damage.
