Overproduction of Tenascin‐C Driven by Lipid Accumulation in the Liver Aggravates Hepatic Ischemia/Reperfusion Injury in Steatotic Mice
Author:
Affiliation:
1. The Dumont‐UCLA Transplant Center, Division of Liver and Pancreas Transplantation, Department of Surgery David Geffen School of Medicine at UCLA, University of California Los Angeles, Los Angeles CA
Funder
National Institute of Allergy and Infectious Diseases
Publisher
Wiley
Subject
Transplantation,Hepatology,Surgery
Link
https://onlinelibrary.wiley.com/doi/pdf/10.1002/lt.25365
Reference50 articles.
1. Neutrophils: a cornerstone of liver ischemia and reperfusion injury
2. Biological modulation of liver ischemia–reperfusion injury
3. The utility of marginal donors in liver transplantation
4. Mechanisms of ischemic injury are different in the steatotic and normal rat liver
5. Endoplasmic reticulum stress is a mediator of posttransplant injury in severely steatotic liver allografts
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