Current Research and Advancements in Liver Ischemia and Reperfusion Injury

A special issue of Journal of Clinical Medicine (ISSN 2077-0383).

Deadline for manuscript submissions: closed (31 May 2017)

Special Issue Editor


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Guest Editor
Department of Surgery, School of Medicine, Faculty of Health Sciences, Aristotle University of Thessaloniki, Thessaloniki, Greece
Interests: liver surgery; liver transplantation; pancreatic surgery; liver and pancreas cancer; HCC; HCC signaling; immunosupression; immunotherapy
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Special Issue Information

Dear Colleagues,

Liver ischemia/reperfusion (I/R) injury occurs during liver transplantation, major hepatectomy when vascular control is needed, and severe hemorrhage when perfusion of the liver is remarkably impaired. Reperfusion injury to the liver may cause primary graft dysfunction, as well as chronic rejection. Several molecules and cells have been implicated in I/R, including elements of the innate immune response, such as reactive oxygen species, cytokines, chemokines, complement, and neutrophils. Generation of reactive oxygen species during reperfusion is believed to contribute to direct injury of the cells in the liver. Accordingly, endothelial cell damage and disturbance of microcirculation and Kupffer cell activation initiate the complex network of proinflammatory signal-transduction cascade. Subsequent recruitment of neutrophils further amplifies tissue damage. Activated Kupffer cells produce and secrete proinflammatory cytokines, including tumor necrosis factor-a (TNFa) and interleukin-1 (IL-1). Production of these cytokines is assumed to be regulated by the transcription factors, Nuclear Factor-κB (NF-κB) and Activating Protein-1 (AP-1), which are activated upon I/R. Multiple signaling cascades, including signal transducer, p38 mitogen-activated protein kinases (MAPKs) and stress activated protein kinase (SAPK) or c-Jun Nterminal kinase (JNK), have been implicated in inflammatory and cell death pathways in the injured liver activated in I/R.

Assoc. Prof. Dimitris E. Giakoustidis
Guest Editor

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Keywords

  • Liver
  • Ischemia
  • Reperfusion
  • Kupffer cells
  • TNFa
  • NF-κB
  • γδTCR
  • JNK
  • IL-17A

Published Papers (2 papers)

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Review
An Evaluation of Ischaemic Preconditioning as a Method of Reducing Ischaemia Reperfusion Injury in Liver Surgery and Transplantation
by Francis P. Robertson, Barry J. Fuller and Brian R. Davidson
J. Clin. Med. 2017, 6(7), 69; https://doi.org/10.3390/jcm6070069 - 14 Jul 2017
Cited by 40 | Viewed by 6941
Abstract
Liver Ischaemia Reperfusion (IR) injury is a major cause of post-operative liver dysfunction, morbidity and mortality following liver resection surgery and transplantation. There are no proven therapies for IR injury in clinical practice and new approaches are required. Ischaemic Preconditioning (IPC) can be [...] Read more.
Liver Ischaemia Reperfusion (IR) injury is a major cause of post-operative liver dysfunction, morbidity and mortality following liver resection surgery and transplantation. There are no proven therapies for IR injury in clinical practice and new approaches are required. Ischaemic Preconditioning (IPC) can be applied in both a direct and remote fashion and has been shown to ameliorate IR injury in small animal models. Its translation into clinical practice has been difficult, primarily by a lack of knowledge regarding the dominant protective mechanisms that it employs. A review of all current studies would suggest that IPC/RIPC relies on creating a small tissue injury resulting in the release of adenosine and l-arginine which act through the Adenosine receptors and the haem-oxygenase and endothelial nitric oxide synthase systems to reduce hepatocyte necrosis and improve the hepatic microcirculation post reperfusion. The next key step is to determine how long the stimulus requires to precondition humans to allow sufficient injury to occur to release the potential mediators. This would open the door to a new therapeutic chapter in this field. Full article
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Review
Natural Killer T Cells in Liver Ischemia–Reperfusion Injury
by Michael A. Zimmerman, Alicia Martin, Jennifer Yee, Jennifer Schiller and Johnny C. Hong
J. Clin. Med. 2017, 6(4), 41; https://doi.org/10.3390/jcm6040041 - 01 Apr 2017
Cited by 15 | Viewed by 4355
Abstract
Restoration of blood flow to an ischemic organ results in significant tissue injury. In the field of liver transplantation, ischemia–reperfusion injury (IRI) has proven to be a formidable clinical obstacle. In addition to metabolic stress and inflammation, IRI results in profound graft dysfunction [...] Read more.
Restoration of blood flow to an ischemic organ results in significant tissue injury. In the field of liver transplantation, ischemia–reperfusion injury (IRI) has proven to be a formidable clinical obstacle. In addition to metabolic stress and inflammation, IRI results in profound graft dysfunction and loss. The severity of IRI further limits the ability to expand the donor pool by using partial grafts and marginal organs. As such, the inflammatory response to reperfusion of the liver continues to be an area of intense investigation. Among the various leukocytes involved in IRI, new insights suggest that natural killer T (NKT) cells may be a central driver of hepatocellular injury. Herein, we examine recent experimental observations that provide a mechanistic link between NKT cell recruitment to liver and post-perfusion tissue injury. Full article
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