Autophagy in ischemic livers: A critical role of sirtuin 1/mitofusin 2 axis in autophagy induction

Sung Kook Chun, Kristina Go, Ming Jim Yang, Ivan Zendejas, Kevin E. Behrns, Jae Sung Kim

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


No-flow ischemia occurs during cardiac arrest, hemorrhagic shock, liver resection and transplantation. Recovery of blood flow and normal physiological pH, however, irreversibly injures the liver and other tissues. Although the liver has the powerful machinery for mitochondrial quality control, a process called mitophagy, mitochondrial dysfunction and subsequent cell death occur after reperfusion. Growing evidence indicates that reperfusion impairs mitophagy, leading to mitochondrial dysfunction, defective oxidative phosphorylation, accumulation of toxic metabolites, energy loss and ultimately cell death. The importance of acetylation/deacetylation cycle in the mitochondria and mitophagy has recently gained attention. Emerging data suggest that sirtuins, enzymes deacetylating a variety of target proteins in cellular metabolism, survival and longevity, may also act as an autophagy modulator. This review highlights recent advances of our understanding of a mechanistic correlation between sirtuin 1, mitophagy and ischemic liver injury.

Original languageEnglish
Pages (from-to)35-46
Number of pages12
JournalToxicological Research
Issue number1
StatePublished - 2016


  • Acetylation
  • Autophagy
  • Ischemia/Reperfusion
  • Liver
  • Mitochondria


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