脂肪变性供肝冷缺血损伤的研究进展

肝移植是治疗终末期肝病的重要手段，然而供者短缺限制了肝移植的发展，如何扩大供肝来源成为学术界的难题。近年来非酒精性脂肪性肝病（NAFLD）供者比例增加，合理利用脂肪变性供肝是扩大供者池的可行方案。肝移植前供肝保存过程的冷缺血损伤增加了术后器官功能不全的发生率。因此了解脂肪变性供肝冷缺血损伤机制和干预措施尤为重要。脂肪变性供肝冷缺血损伤在细胞器层面具体表现为线粒体、溶酶体、内质网的损伤，蛋白层面主要表现腺苷酸活化蛋白激酶（AMPK）、乙醛脱氢酶2（ALDH2）、血红素加氧酶（HO）-1的表达增加。本文就脂肪变性供肝冷缺血损伤的研究进展及相关干预措施做一综述。

Research progress on cold ischemia injury of steatotic donor livers

Liver transplantation is a vital treatment for end-stage liver disease. However, the shortage of donor livers has limited the development of liver transplantation. How to expand the source of donor livers has become a challenge in the academic community. In recent years, the proportion of donors with non-alcoholic fatty liver disease (NAFLD) has been increased. Rational use of steatotic donor livers is a feasible approach to expand the donor pool. Cold ischemia injury during donor liver preservation before liver transplantation increases the risk of postoperative organ dysfunction. Therefore, it is of significance to unravel the mechanism and intervention measures of cold ischemia injury of steatotic donor livers. Cold ischemia injury of steatotic donor livers is characterized as the damage of mitochondria, lysosomes and endoplasmic reticulum at the organelle level, and up-regulated expression of adenosine monphosphate activated protein kinase (AMPK), aldehyde dehydrogenase 2 (ALDH2) and heme oxygenase (HO)-1 at the protein level. In this article, the research progresses on cold ischemia injury of steatotic donor livers and relevant intervention measures were reviewed.