A New Approach to Mitigate Donor Liver Ischemia/Reperfusion Injury

Liver transplantation remains the most effective treatment option for patients with end-stage liver disease. However, the demand for liver transplants far exceeds the supply of organs, so improving the quality of the donor liver in advance can effectively alleviate this phenomenon. Yazdani et al1 found that exercise preconditioning of mice for 4 wk inhibited apoptosis, suppressed neutrophil infiltration, and promoted PGC-1α expression and mitochondrial content in the liver. This study suggests that the exercise of the donor can attenuate cold ischemia/reperfusion injury (IRI), and this study is of great significance for expanding the choice of marginal donors and improving the quality of donor livers. At the same time, we have several questions about this article: First, mice are usually active and aggressive; how could you ensure that mice remained sedentary? Second, the authors mentioned neutrophil alterations were evident 6 h after liver transplantation. What is the basis for the 6 h, and how do B lymphocytes, T lymphocytes, and dendritic cells play a role in this part? Third, In recent years, the incidence of obesity has increased with dietary changes, and the proportion of nonalcoholic fatty liver disease in the donor pool has increased over the years. The rational and selective application of fatty liver as a donor remains an effective alternative to meet the transplantation needs of patients.2 IRI is aggravated in fatty livers compared with normal livers, mainly due to impaired reflux and overproduction of reactive oxygen species.3,4 Inhibition of PGC-1α has been found to aggravate IRI in fatty liver.5 Can the same effect be achieved if exercise treats the fatty liver, and if so, what difference does the mechanism make?