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
Interests: liver surgery; liver transplantation; pancreatic surgery; liver and pancreas cancer; HCC; HCC signaling; immunosupression; immunotherapy
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
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
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