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논문 기본 정보

자료유형
학술저널
저자정보
Sung Kook Chun (University of Florida) Kristina Go (University of Florida) Ming-Jim Yang (University of Florida) Ivan Zendejas (University of Florida) Kevin E. Behrns (University of Florida) Jae-Sung Kim (University of Florida)
저널정보
한국독성학회 Toxicological Research Toxicological Research Vol.32 No.1
발행연도
2016.1
수록면
35 - 46 (12page)

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초록· 키워드

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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.

목차

INTRODUCTION
THE LIVER
LIVER SURGERY AND I/R INJURY
MECHANISMS OF I/R INJURY
AUTOPHAGY
MITOPHAGY
MITOPHAGY IN LIVER I/R INJURY
SIRTUINS IN THE LIVER
ROLE OF ACETYLATION/DEACETYLATION IN AUTOPHAGY
SIRT1, AUTOPHAGY AND I/R INJURY
CONCLUSION AND FUTURE PERSPECTIVES
REFERENCES

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UCI(KEPA) : I410-ECN-0101-2016-513-002333910