Liver ischemia/reperfusion injury: Processes in inflammatory networks—A review

Authors

  • Mahmoud Abu-Amara,

    1. Liver Transplantation and Hepatobiliary Unit, Royal Free Hospital, London, United Kingdom
    2. Division of Surgery and Interventional Science, University College London, London, United Kingdom
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  • Shi Yu Yang,

    1. Division of Surgery and Interventional Science, University College London, London, United Kingdom
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  • Niteen Tapuria,

    1. Liver Transplantation and Hepatobiliary Unit, Royal Free Hospital, London, United Kingdom
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  • Barry Fuller,

    1. Division of Surgery and Interventional Science, University College London, London, United Kingdom
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  • Brian Davidson,

    1. Liver Transplantation and Hepatobiliary Unit, Royal Free Hospital, London, United Kingdom
    2. Division of Surgery and Interventional Science, University College London, London, United Kingdom
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  • Alexander Seifalian

    Corresponding author
    1. Liver Transplantation and Hepatobiliary Unit, Royal Free Hospital, London, United Kingdom
    2. Division of Surgery and Interventional Science, University College London, London, United Kingdom
    • University College London, Pond Street, London NW3 2QG, United Kingdom
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    • Telephone: +44 20 7830 2901; FAX: 020 7472 6444


Abstract

Liver ischemia/reperfusion (IR) injury is typified by an inflammatory response. Understanding the cellular and molecular events underpinning this inflammation is fundamental to developing therapeutic strategies. Great strides have been made in this respect recently. Liver IR involves a complex web of interactions between the various cellular and humoral contributors to the inflammatory response. Kupffer cells, CD4+ lymphocytes, neutrophils, and hepatocytes are central cellular players. Various cytokines, chemokines, and complement proteins form the communication system between the cellular components. The contribution of the danger-associated molecular patterns and pattern recognition receptors to the pathophysiology of liver IR injury are slowly being elucidated. Our knowledge on the role of mitochondria in generating reactive oxygen and nitrogen species, in contributing to ionic disturbances, and in initiating the mitochondrial permeability transition with subsequent cellular death in liver IR injury is continuously being expanded. Here, we discuss recent findings pertaining to the aforementioned factors of liver IR, and we highlight areas with gaps in our knowledge, necessitating further research. Liver Transpl 16:1016–1032, 2010. © 2010 AASLD.

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