TY - JOUR
TI - Pathophysiological changes during ischemia-reperfusion injury in rodent hepatic steatosis
AU - Neri, A.-A.
AU - Dontas, I.A.
AU - Iliopoulos, D.C.
AU - Karatzas, T.
JO - In vivo (Athens, Greece)
PY - 2020
VL - 34
TODO - 3
SP - 953-964
PB - International Institute of Anticancer Research
SN - null
TODO - 10.21873/invivo.11863
TODO - caspase;  chaperone;  glutathione;  interleukin 10;  interleukin 1alpha;  interleukin 1beta;  interleukin 6;  nitric oxide;  reactive oxygen metabolite;  selectin (glycoprotein);  tumor necrosis factor;  cytokine, apoptosis;  cell death;  endoplasmic reticulum;  fatty liver;  hepatic ischemia reperfusion injury;  histopathology;  human;  ischemia;  Kupffer cell;  microcirculation;  nonhuman;  pathophysiology;  Review;  adverse event;  animal;  complication;  diet restriction;  disease model;  liver resection;  liver transplantation;  metabolism;  nonalcoholic fatty liver;  oxidative stress;  procedures;  reperfusion injury;  rodent, Animals;  Cytokines;  Disease Models, Animal;  Fasting;  Hepatectomy;  Liver Transplantation;  Microcirculation;  Non-alcoholic Fatty Liver Disease;  Oxidative Stress;  Reperfusion Injury;  Rodentia
TODO - Background/Aim: Ischemia and reperfusion injuries may produce deleterious effects on hepatic tissue after liver surgery and transplantation. The impact of ischemia-reperfusion injury (ΙRΙ) on the liver depends on its substrate, the percentage of liver ischemic tissue subjected to IRI and the ischemia time. The consequences of IRI are more evident in pathologic liver substrates, such as steatotic livers. This review is the result of an extended bibliographic PubMed search focused on the last 20 years. It highlights basic differences encountered during IRI in lean and steatotic livers based on studies using rodent experimental models. Conclusion: The main difference in cell death between lean and steatotic livers is the prevalence of apoptosis in the former and necrosis in the latter. There are also major changes in the effect of intracellular mediators, such as TNFα and IL-1β. Further experimental studies are needed in order to increase current knowledge of IRI effects and relevant mechanisms in both lean and steatotic livers, so that new preventive and therapeutic strategies maybe developed. © 2020 International Institute of Anticancer Research. All rights reserved.
ER -