Ischemia/reperfusion (I/R) injury inevitably occurs during liver resection and transplantation. Elderly patients poorly recover from these surgeries. This reduced reparative capacity with aging is causatively associated with decreased mitochondrial function after reperfusion. Mitochondrial autophagy (mitophagy) is a vital cellular process that timely clears abnormal and dysfunctional mitochondria. Impaired or insufficient autophagy can contribute to hepatocyte death after I/R. This review describes our current understanding of I/R injury and highlights new mechanistic correlation between sirtuin 1 (SIRT1), mitofusin 2 (MFN2), and autophagy in the pathogenesis of age-dependent hypersensitivity to reperfusion injury. The deacetylation of MFN2 by SIRT1 plays a pivotal role in the recovery from reperfusion injury by modulating the onset of autophagy. Targeting the SIRT1-MFN2 axis could be a new therapeutic target to reduce I/R injury in aged livers.

Original languageEnglish
Pages (from-to)133-137
Number of pages5
JournalLiver Research
Issue number3
StatePublished - Sep 2018


  • Aging
  • Autophagy
  • Hepatocytes
  • Ischemia/reperfusion (I/R)
  • Mitochondrial autophagy (mitophagy)
  • Sirtuin 1-mitofusin 2 (SIRT1-MFN2) axis


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