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Autophagy and liver ischemia-reperfusion injury (pp.297-328) $0.00
Authors:  (Raffaele Cursio, Pascal Colosetti, Patrick Auberger, Jean Gugenheim)
Abstract:
Liver ischemia-reperfusion (I-R) injury occurs during hemorrhagic shock and liver surgery, particularly during liver transplantation. After liver transplantation, I-R injury causes up to 10% of early transplant failures and can lead to acute and chronic rejection. Originally, the mode of cell death after I-R was considered to be necrotic, then it was shown that apoptosis too plays an important role, and now there is increasing evidence that autophagy is also involved. Autophagy is a conserved cellular process that controls protein and organelle degradation and recycling, and has essential roles in survival, development and homeostasis. Thus autophagy is involved in physiology, lifespan and a wide range of diseases, including cancer, neurodegeneration and microbial infection. In the normal liver, autophagy is enhanced in starved animals or following glucagon infusion. During Hepatitis B and C infections, acute liver injury and alpha1-antitrypsin deficit autophagy is increased; whereas in the alcoholic or steatotic liver and in hepatocellular carcinoma it is decreased. Modulation of autophagy by its inhibitors and/or stimulators may reduce liver I-R injury during liver surgery.
The objectives of this chapter are to provide a review of the mechanisms mediating I-R liver injury in experimental and clinical settings with particular focus on the role of autophagy, its interconnection with apoptosis and necrosis and, finally to summarize the
most promising surgical and pharmacological autophagy target therapies ameliorating sequelae of the I-R injury. 


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Autophagy and liver ischemia-reperfusion injury (pp.297-328)