Ischemia-free liver transplantation improves the prognosis of recipients using functionally marginal liver grafts

Autor: Shuai Wang, Xiaohong Lin, Yunhua Tang, Yichen Liang, Min Zhang, Zhonghao Xie, Yiwen Guo, Yuqi Dong, Qiang Zhao, Zhiyong Guo, Dongping Wang, Xiaoshun He, Weiqiang Ju, Maogen Chen
Jazyk: angličtina
Rok vydání: 2024
Předmět:
Zdroj: Clinical and Molecular Hepatology, Vol 30, Iss 3, Pp 421-435 (2024)
Druh dokumentu: article
ISSN: 2287-2728
2287-285X
DOI: 10.3350/cmh.2024.0139
Popis: Background/Aims The shortage of donor liver hinders the development of liver transplantation. This study aimed to clarify the poor outcomes of functionally marginal liver grafts (FMLs) and provide evidence for the improvement of ischemia-free liver transplantation (IFLT) after FML transplantation. Methods Propensity score matching was used to control for confounding factors. The outcomes of the control group and FML group were compared to demonstrate the negative impact of FMLs on liver transplantation patients. We compared the clinical improvements of the different surgical types. To elucidate the underlying mechanism, we conducted bioinformatic analysis based on transcriptome and single-cell profiles. Results FMLs had a significantly greater hazard ratio (HR: 1.969, P=0.018) than did other marginal livers. A worse 90-day survival (Mortality: 12.3% vs. 5.0%, P=0.007) was observed in patients who underwent FML transplantation. Patients who received FMLs had a significant improvement in overall survival after IFLT (Mortality: 10.4% vs 31.3%, P=0.006). Pyroptosis and inflammation were inhibited in patients who underwent IFLT. The infiltration of natural killer cells was lower in liver grafts from these patients. Bulk transcriptome profiles revealed a positive relationship between IL-32 and Caspase 1 (R=0.73, P=0.01) and between IL-32 and Gasdermin D (R=0.84, P=0.0012). Conclusions FML is a more important negative prognostic parameter than other marginal liver parameters. IFLT might ameliorate liver injury in FMLs by inhibiting the infiltration of NK cells, consequently leading to the abortion of IL-32, which drives pyroptosis in monocytes and macrophages.
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