Ischaemia reperfusion injury in liver transplantation: Cellular and molecular mechanisms

Liver disease causing end organ failure is a growing cause of mortality. In most cases, the only therapy is liver transplantation. However, liver transplantation is a complex undertaking and its success is dependent on a number of factors. In particular, liver transplantation is subject to the risks...

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Published inLiver international Vol. 39; no. 5; pp. 788 - 801
Main Authors Dar, Wasim A., Sullivan, Elise, Bynon, John S., Eltzschig, Holger, Ju, Cynthia
Format Journal Article
LanguageEnglish
Published United States Wiley Subscription Services, Inc 01.05.2019
Subjects
Activation
Autophagy
Endothelial cells
Gene expression
Health risks
Hepatocytes
Hypoxia
hypoxia‐inducible factors
ischaemia reperfusion
Ischemia
Kupffer cells
Leukocytes (neutrophilic)
Liver
Liver diseases
Liver transplantation
Molecular modelling
Phagocytosis
Platelets
Reperfusion
Ribonucleic acid
Risk analysis
Risk factors
RNA
Signal transduction
Steatosis
therapeutics
Toll-like receptors
Transplantation
hypoxia-inducible factors
therapeutics
ischaemia reperfusion
liver transplantation
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Abstract Liver disease causing end organ failure is a growing cause of mortality. In most cases, the only therapy is liver transplantation. However, liver transplantation is a complex undertaking and its success is dependent on a number of factors. In particular, liver transplantation is subject to the risks of ischaemia‐reperfusion injury (IRI). Liver IRI has significant effects on the function of a liver after transplantation. The cellular and molecular mechanisms governing IRI in liver transplantation are numerous. They involve multiple cells types such as liver sinusoidal endothelial cells, hepatocytes, Kupffer cells, neutrophils and platelets acting via an interconnected network of molecular pathways such as activation of toll‐like receptor signalling, alterations in micro‐RNA expression, production of ROS, regulation of autophagy and activation of hypoxia‐inducible factors. Interestingly, the cellular and molecular events in liver IRI can be correlated with clinical risk factors for IRI in liver transplantation such as donor organ steatosis, ischaemic times, donor age, and donor and recipient coagulopathy. Thus, understanding the relationship of the clinical risk factors for liver IRI to the cellular and molecular mechanisms that govern it is critical to higher levels of success after liver transplantation. This in turn will help in the discovery of therapeutics for IRI in liver transplantation – a process that will lead to improved outcomes for patients suffering from end‐stage liver disease.
AbstractList Liver disease causing end organ failure is a growing cause of mortality. In most cases, the only therapy is liver transplantation. However, liver transplantation is a complex undertaking and its success is dependent on a number of factors. In particular, liver transplantation is subject to the risks of ischaemia‐reperfusion injury (IRI). Liver IRI has significant effects on the function of a liver after transplantation. The cellular and molecular mechanisms governing IRI in liver transplantation are numerous. They involve multiple cells types such as liver sinusoidal endothelial cells, hepatocytes, Kupffer cells, neutrophils and platelets acting via an interconnected network of molecular pathways such as activation of toll‐like receptor signalling, alterations in micro‐RNA expression, production of ROS, regulation of autophagy and activation of hypoxia‐inducible factors. Interestingly, the cellular and molecular events in liver IRI can be correlated with clinical risk factors for IRI in liver transplantation such as donor organ steatosis, ischaemic times, donor age, and donor and recipient coagulopathy. Thus, understanding the relationship of the clinical risk factors for liver IRI to the cellular and molecular mechanisms that govern it is critical to higher levels of success after liver transplantation. This in turn will help in the discovery of therapeutics for IRI in liver transplantation – a process that will lead to improved outcomes for patients suffering from end‐stage liver disease.
Liver disease causing end organ failure is a growing cause of mortality. In most cases, the only therapy is liver transplantation. However, liver transplantation is a complex undertaking and its success is dependent on a number of factors. In particular, liver transplantation is subject to the risks of ischaemia-reperfusion injury (IRI). Liver IRI has significant effects on the function of a liver after transplantation. The cellular and molecular mechanisms governing IRI in liver transplantation are numerous. They involve multiple cells types such as liver sinusoidal endothelial cells, hepatocytes, Kupffer cells, neutrophils and platelets acting via an interconnected network of molecular pathways such as activation of toll-like receptor signalling, alterations in micro-RNA expression, production of ROS, regulation of autophagy and activation of hypoxia-inducible factors. Interestingly, the cellular and molecular events in liver IRI can be correlated with clinical risk factors for IRI in liver transplantation such as donor organ steatosis, ischaemic times, donor age, and donor and recipient coagulopathy. Thus, understanding the relationship of the clinical risk factors for liver IRI to the cellular and molecular mechanisms that govern it is critical to higher levels of success after liver transplantation. This in turn will help in the discovery of therapeutics for IRI in liver transplantation - a process that will lead to improved outcomes for patients suffering from end-stage liver disease.Liver disease causing end organ failure is a growing cause of mortality. In most cases, the only therapy is liver transplantation. However, liver transplantation is a complex undertaking and its success is dependent on a number of factors. In particular, liver transplantation is subject to the risks of ischaemia-reperfusion injury (IRI). Liver IRI has significant effects on the function of a liver after transplantation. The cellular and molecular mechanisms governing IRI in liver transplantation are numerous. They involve multiple cells types such as liver sinusoidal endothelial cells, hepatocytes, Kupffer cells, neutrophils and platelets acting via an interconnected network of molecular pathways such as activation of toll-like receptor signalling, alterations in micro-RNA expression, production of ROS, regulation of autophagy and activation of hypoxia-inducible factors. Interestingly, the cellular and molecular events in liver IRI can be correlated with clinical risk factors for IRI in liver transplantation such as donor organ steatosis, ischaemic times, donor age, and donor and recipient coagulopathy. Thus, understanding the relationship of the clinical risk factors for liver IRI to the cellular and molecular mechanisms that govern it is critical to higher levels of success after liver transplantation. This in turn will help in the discovery of therapeutics for IRI in liver transplantation - a process that will lead to improved outcomes for patients suffering from end-stage liver disease.
Author Ju, Cynthia
Sullivan, Elise
Bynon, John S.
Eltzschig, Holger
Dar, Wasim A.
Author_xml – sequence: 1
  givenname: Wasim A.
  orcidid: 0000-0001-8095-248X
  surname: Dar
  fullname: Dar, Wasim A.
  email: wasim.a.dar@uth.tmc.edu
  organization: McGovern Medical School at UT Health
– sequence: 2
  givenname: Elise
  surname: Sullivan
  fullname: Sullivan, Elise
  organization: McGovern Medical School at UT Health
– sequence: 3
  givenname: John S.
  surname: Bynon
  fullname: Bynon, John S.
  organization: McGovern Medical School at UT Health
– sequence: 4
  givenname: Holger
  surname: Eltzschig
  fullname: Eltzschig, Holger
  organization: McGovern Medical School at UT Health
– sequence: 5
  givenname: Cynthia
  surname: Ju
  fullname: Ju, Cynthia
  organization: McGovern Medical School at UT Health
BackLink https://www.ncbi.nlm.nih.gov/pubmed/30843314$$D View this record in MEDLINE/PubMed
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Issue 5
Keywords hypoxia-inducible factors
therapeutics
ischaemia reperfusion
liver transplantation
Language English
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H. Eltzschig, NIH NHLBI (R01HL119837, R01HL133900); C. Ju NIH NIAAA (U01AA021723, R21AA024636), NIDDK (R01DK109574).
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Snippet Liver disease causing end organ failure is a growing cause of mortality. In most cases, the only therapy is liver transplantation. However, liver...
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SubjectTerms Activation
Autophagy
Endothelial cells
Gene expression
Health risks
Hepatocytes
Hypoxia
hypoxia‐inducible factors
ischaemia reperfusion
Ischemia
Kupffer cells
Leukocytes (neutrophilic)
Liver
Liver diseases
Liver transplantation
Molecular modelling
Phagocytosis
Platelets
Reperfusion
Ribonucleic acid
Risk analysis
Risk factors
RNA
Signal transduction
Steatosis
therapeutics
Toll-like receptors
Transplantation
Title Ischaemia reperfusion injury in liver transplantation: Cellular and molecular mechanisms
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fliv.14091
https://www.ncbi.nlm.nih.gov/pubmed/30843314
https://www.proquest.com/docview/2213749673
https://www.proquest.com/docview/2188986000
Volume 39
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