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.

Protocol for the pig liver ischemia/reperfusion injury

2020 ◽  
Author(s):  
Eric Felli ◽  
Mahdi Al-Taher ◽  
Emanuele Felli ◽  
Lorenzo Cinelli ◽  
Michele Diana
Keyword(s):  
Liver Transplantation ◽  
Reperfusion Injury ◽  
Liver Damage ◽  
Porcine Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Graft Loss ◽  
Vascular Complication ◽  
Liver Ischemia ◽  
Pig Liver

Abstract Liver ischemia/reperfusion injury (IRI) is a dreadful vascular complication, which leads to liver damage. It is often associated with graft loss in liver transplantation and with a higher morbidity and mortality. IRI can have different causes, such as inflow clumping during surgical procedures in hepatic resection, liver transplantation, trauma, as well as during the stenosis of the vasculature caused by cancer. Here, we show a detailed IRI protocol in a porcine model.

scholarly journals Beyond Preconditioning: Postconditioning as an Alternative Technique in the Prevention of Liver Ischemia-Reperfusion Injury

2016 ◽  
Vol 2016 ◽  
pp. 1-21 ◽  
Author(s):  
Kassiani Theodoraki ◽  
Iosifina Karmaniolou ◽  
Aliki Tympa ◽  
Marios-Konstantinos Tasoulis ◽  
Constantinos Nastos ◽  
...  
Keyword(s):  
Blood Flow ◽  
Reperfusion Injury ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Liver Ischemia ◽  
Neutrophil Accumulation ◽  
Postoperative Function ◽  
Early Reperfusion ◽  
And Function

Liver ischemia/reperfusion injury may significantly compromise hepatic postoperative function. Various hepatoprotective methods have been improvised, aiming at attenuating IR injury. With ischemic preconditioning (IPC), the liver is conditioned with a brief ischemic period followed by reperfusion, prior to sustained ischemia. Ischemic postconditioning (IPostC), consisting of intermittent sequential interruptions of blood flow in the early phase of reperfusion, seems to be a more feasible alternative than IPC, since the onset of reperfusion is more predictable. Regarding the potential mechanisms involved, it has been postulated that the slow intermittent oxygenation through controlled reperfusion decreases the burst production of oxygen free radicals, increases antioxidant activity, suppresses neutrophil accumulation, and modulates the apoptotic cascade. Additionally, favorable effects on mitochondrial ultrastructure and function, and upregulation of the cytoprotective properties of nitric oxide, leading to preservation of sinusoidal structure and maintenance of blood flow through the hepatic circulation could also underlie the protection afforded by postconditioning. Clinical studies are required to show whether biochemical and histological improvements afforded by the reperfusion/reocclusion cycles of postconditioning during early reperfusion can be translated to a substantial clinical benefit in liver resection and transplantation settings or to highlight more aspects of its molecular mechanisms.

Molecular mechanisms of hepatic ischemia-reperfusion injury and preconditioning

2003 ◽  
Vol 284 (1) ◽  
pp. G15-G26 ◽  
Author(s):  
Hartmut Jaeschke
Keyword(s):  
Reperfusion Injury ◽  
Liver Surgery ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion Injury ◽  
Current Knowledge ◽  
Ischemia Reperfusion ◽  
Oxidant Stress ◽  
Cellular Mechanisms ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion

Ischemia-reperfusion injury is, at least in part, responsible for the morbidity associated with liver surgery under total vascular exclusion or after liver transplantation. The pathophysiology of hepatic ischemia-reperfusion includes a number of mechanisms that contribute to various degrees in the overall injury. Some of the topics discussed in this review include cellular mechanisms of injury, formation of pro- and anti-inflammatory mediators, expression of adhesion molecules, and the role of oxidant stress during the inflammatory response. Furthermore, the roles of nitric oxide in preventing microcirculatory disturbances and as a substrate for peroxynitrite formation are reviewed. In addition, emerging mechanisms of protection by ischemic preconditioning are discussed. On the basis of current knowledge, preconditioning or pharmacological interventions that mimic these effects have the greatest potential to improve clinical outcome in liver surgery involving ischemic stress and reperfusion.

A Novel and Sensitive Approach for the Evaluation of Liver Ischemia-Reperfusion Injury After Liver Transplantation

2016 ◽  
Vol 51 (3) ◽  
pp. 170-176 ◽  
Author(s):  
Martina Brandlhuber ◽  
Marco Armbruster ◽  
Blaž Zupanc ◽  
Paola Coan ◽  
Emmanuel Brun ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Liver Ischemia

scholarly journals Autophagy and Liver Ischemia-Reperfusion Injury

2015 ◽  
Vol 2015 ◽  
pp. 1-16 ◽  
Author(s):  
Raffaele Cursio ◽  
Pascal Colosetti ◽  
Jean Gugenheim
Keyword(s):  
Cell Death ◽  
Hemorrhagic Shock ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Current Knowledge ◽  
Ischemia Reperfusion ◽  
Liver Ischemia ◽  
Main Mode ◽  
Patient Morbidity ◽  
Diseased Liver

Liver ischemia-reperfusion (I-R) injury occurs during liver resection, liver transplantation, and hemorrhagic shock. The main mode of liver cell death after warm and/or cold liver I-R is necrosis, but other modes of cell death, as apoptosis and autophagy, are also involved. Autophagy is an intracellular self-digesting pathway responsible for removal of long-lived proteins, damaged organelles, and malformed proteins during biosynthesis by lysosomes. Autophagy is found in normal and diseased liver. Although depending on the type of ischemia, warm and/or cold, the dynamic process of liver I-R results mainly in adenosine triphosphate depletion and in production of reactive oxygen species (ROS), leads to both, a local ischemic insult and an acute inflammatory-mediated reperfusion injury, and results finally in cell death. This process can induce liver dysfunction and can increase patient morbidity and mortality after liver surgery and hemorrhagic shock. Whether autophagy protects from or promotes liver injury following warm and/or cold I-R remains to be elucidated. The present review aims to summarize the current knowledge in liver I-R injury focusing on both the beneficial and the detrimental effects of liver autophagy following warm and/or cold liver I-R.

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
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