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- Jiang Liu, Li Pang, NgKevin T PKTPDepartment of Surgery, HKU-Shenzhen Hospital & Department of Surgery, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong, China; and., T L Shirley Chiu, Hui Liu, Xiaobing Liu, Aimin Xu, Chung-Mau Lo, and Kwan Man.
- Department of Surgery, HKU-Shenzhen Hospital & Department of Surgery, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong, China; and.
- Ann. Surg. 2022 Nov 1; 276 (5): e483-e492.
ObjectiveTo investigate the association of graft steatosis with long-term outcome, and to elucidate the mechanism of steatotic graft injury in adult living donor liver transplantation.Summary Of Background DataThe utilization of steatotic graft expands the donor pool for living donor liver transplantation (LDLT). However, it remains controversial due to its high morbidity and mortality. Elucidating the mechanism of steatotic graft injury is crucial to develop therapeutic strategies targeting at graft injury and to further expand the donor pool.MethodsFive hundred thirty patients receiving LDLT were prospectively included for risk factor analysis and outcome comparison. Rat orthotopic liver transplantation, in vitro functional experiments and mouse hepatic ischemia/ reperfusion models were established to explore the mechanisms of steatotic graft injury.ResultsWe identified that graft with >10% steatosis was an independent risk factor for long-term graft loss after LDLT (hazard ratio 2.652, P = 0.001), and was associated with shorter cancer recurrence-free survival and acute phase liver injury. Steatotic graft displayed distinct mitochondrial dysfunction, including membrane, calcium, and energy homeostasis dysregulation. Specifically, the mitochondrial biogenesis was remarkably downregulated in steatotic graft. Inhibition of AMPK-PGC1α axis impaired mitochondrial biogenesis and was lethal to fatty hepatocyte in vitro , whereas reactivation of AMPK promoted PGC1α-mediated mitochondrial biogenesis and attenuated liver injury via restoring mitochondrial function in animal model. Conclusions: We provided a new mechanism that compromised AMPK-PGC1α axis exacerbated steatotic graft injury in LDLT by dysregulating mitochondrial homeostasis through impairment of biogenesis.Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.
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