scholarly journals Cellular and molecular mechanisms of abnormal calcification following ischemia–reperfusion injury in human liver transplantation

2007 ◽  
Vol 20 (3) ◽  
pp. 357-366 ◽  
Author(s):  
Fariba Kalantari ◽  
Dengshun Miao ◽  
Anouk Emadali ◽  
George N Tzimas ◽  
David Goltzman ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Reperfusion Injury ◽  
Human Liver ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion

scholarly journals Disulfide High‐Mobility Group Box 1 Drives Ischemia‐Reperfusion Injury in Human Liver Transplantation

Hepatology ◽  
2020 ◽  
Author(s):  
Rebecca A. Sosa ◽  
Allyson Q. Terry ◽  
Fady M. Kaldas ◽  
Yi‐Ping Jin ◽  
Maura Rossetti ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Reperfusion Injury ◽  
Human Liver ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
High Mobility ◽  
High Mobility Group

scholarly journals Inflammasome-Mediated Inflammation in Liver Ischemia-Reperfusion Injury

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1131 ◽  
Author(s):  
Mónica B. Jiménez-Castro ◽  
María Eugenia Cornide-Petronio ◽  
Jordi Gracia-Sancho ◽  
Carmen Peralta
Keyword(s):  
Liver Transplantation ◽  
Reperfusion Injury ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion Injury ◽  
Current Knowledge ◽  
Ischemia Reperfusion ◽  
Therapeutic Strategies ◽  
Experimental Models ◽  
Inflammasome Activation ◽  
Liver Ischemia

Ischemia-reperfusion injury is an important cause of liver damage occurring during surgical procedures including hepatic resection and liver transplantation, and represents the main underlying cause of graft dysfunction and liver failure post-transplantation. To date, ischemia-reperfusion injury is an unsolved problem in clinical practice. In this context, inflammasome activation, recently described during ischemia-reperfusion injury, might be a potential therapeutic target to mitigate the clinical problems associated with liver transplantation and hepatic resections. The present review aims to summarize the current knowledge in inflammasome-mediated inflammation, describing the experimental models used to understand the molecular mechanisms of inflammasome in liver ischemia-reperfusion injury. In addition, a clear distinction between steatotic and non-steatotic livers and between warm and cold ischemia-reperfusion injury will be discussed. Finally, the most updated therapeutic strategies, as well as some of the scientific controversies in the field will be described. Such information may be useful to guide the design of better experimental models, as well as the effective therapeutic strategies in liver surgery and transplantation that can succeed in achieving its clinical application.

scholarly journals Wide gene expression profiling of ischemia-reperfusion injury in human liver transplantation

2006 ◽  
Vol 13 (1) ◽  
pp. 99-113 ◽  
Author(s):  
Anna Conti ◽  
Simona Scala ◽  
Paola D'Agostino ◽  
Elena Alimenti ◽  
Daniele Morelli ◽  
...  
Keyword(s):  
Gene Expression ◽  
Liver Transplantation ◽  
Reperfusion Injury ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Human Liver ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion

scholarly journals Proteomic Analysis of Ischemia-Reperfusion Injury upon Human Liver Transplantation Reveals the Protective Role of IQGAP1

2006 ◽  
Vol 5 (7) ◽  
pp. 1300-1313 ◽  
Author(s):  
Anouk Emadali ◽  
Béatrice Muscatelli-Groux ◽  
Frédéric Delom ◽  
Sarah Jenna ◽  
Daniel Boismenu ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Reperfusion Injury ◽  
Proteomic Analysis ◽  
Human Liver ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Protective Role

scholarly journals Endogenous Interleukin-33 Acts as an Alarmin in Liver Ischemia-Reperfusion and Is Associated With Injury After Human Liver Transplantation

2021 ◽  
Vol 12 ◽  
Author(s):  
Louise Barbier ◽  
Aurélie Robin ◽  
Rémy Sindayigaya ◽  
Héloïse Ducousso ◽  
Fanny Dujardin ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Renal Failure ◽  
Mouse Model ◽  
Reperfusion Injury ◽  
Human Liver ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Graft Dysfunction ◽  
Hepatic Ischemia ◽  
Transplant Patients

Ischemia and reperfusion injury is an early inflammatory process during liver transplantation that impacts on graft function and clinical outcomes. Interleukin (IL)-33 is a danger-associated molecular pattern involved in kidney ischemia/reperfusion injury and several liver diseases. The aims were to assess whether IL-33 was released as an alarmin responsible for ischemia/reperfusion injury in a mouse model of warm hepatic ischemia, and whether this hypothesis could also apply in the setting of human liver transplantation. First, a model of warm hepatic ischemia/reperfusion was used in wild-type and IL-33–deficient mice. Severity of ischemia/reperfusion injury was assessed with ALT and histological analysis. Then, serum IL-33 was measured in a pilot cohort of 40 liver transplant patients. Hemodynamic postreperfusion syndrome, graft dysfunction (assessed by model for early allograft scoring >6), renal failure, and tissue lesions on time-zero biopsies were assessed. In the mouse model, IL-33 was constitutively expressed in the nucleus of endothelial cells, immediately released in response to hepatic pedicle clamping without neosynthesis, and participated in the recruitment of neutrophils and tissue injury on site. The kinetics of IL-33 in liver transplant patients strikingly matched the ones in the animal model, as attested by serum levels reaching a peak immediately after reperfusion, which correlated to clinical outcomes including postreperfusion syndrome, posttransplant renal failure, graft dysfunction, and histological lesions of ischemia/reperfusion injury. IL-33 was an independent factor of graft dysfunction with a cutoff of IL-33 at 73 pg/ml after reperfusion (73% sensitivity, area under the curve of 0.76). Taken together, these findings establish the immediate implication of IL-33 acting as an alarmin in liver I/R injury and provide evidence of its close association with cardinal features of early liver injury-associated disorders in LT patients.

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