Ischemia-Reperfusion Injury Associated with Liver Transplantation in 2011: Past and Future

Elias-Miró, M.; Jiménez‐Castro, Mónica B.; Peralta, Carmen A.

doi:10.5772/28586

Cited by 4 publications

(5 citation statements)

References 152 publications

(262 reference statements)

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“…The ischemia/reperfusion causes the hepatic neutrophil accumulation. In addition, the Kupffer cells become activated and release proinflammatory cytokines such as reactive oxygen species and the tumor necrosis factor (TNF-α) and IL-1 (3,4). These cytokines activate most of the proteins involved in apoptosis, such as caspase-3 and caspase-9, bcl-2/bax ratio, as well as mitochondria cytochrome-c released to cytoplasm.…”

Section: Introductionmentioning

confidence: 99%

Protective effects of St. John’s wort in the hepatic ischemia/reperfusion injury in rats

et al. 2018

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Section: Introductionmentioning

confidence: 99%

Protective effects of St. John’s wort in the hepatic ischemia/reperfusion injury in rats

et al. 2018

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“…However, the fact that scientific research relies on the use of cell cultures and animal models, sets limitations on improving our knowledge on this subject, as most human tissues are not routinely accessible for research purposes. Despite the aforementioned difficulties, several methods about protecting the liver from IRI have been developed and tested in animal experimental models and significant efforts have been made to apply the results of these studies into clinical practice ( 1 ).…”

Section: Resultsmentioning

confidence: 99%

“…Ischemia reperfusion injury (IRI) is defined as the phenomenon during which cellular damage in an organ, caused by hypoxia, is paradoxically exacerbated after the restoration of oxygen delivery ( 1 ). It is a dynamic process which involves the two interrelated phases of local ischemic insult and inflammation-mediated reperfusion injury ( 2 ).…”

Section: Contextmentioning

confidence: 99%

Hepatic Ischemia and Reperfusion Injury and Trauma: Current Concepts

et al. 2013

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ContextIschemia-reperfusion injury is a fascinating topic which has drawn a lot of interest in the last several years. Hepatic ischemia reperfusion injury may occur in a variety of clinical situations. These include transplantation, liver resection, trauma, and vascular surgery.Evidence AcquisitionThe purpose of this review was to outline the molecular mechanisms underlying hepatic I/R injury and present the latest approaches, both surgical and pharmacological, regarding the prevention of it. A comprehensive electronic literature search in MEDLINE/PubMed was performed to identify relative articles published within the last 2 years.ResultsThe basic mechanism of hepatic ischemia – reperfusion injury is one of blood deprivation during ischemia, followed by the return of flow during reperfusion. It involves a complex series of events, such as mitochondrial deenergization, adenosine-5'-triphosphate depletion, alterations of electrolyte homeostasis, as well as Kupffer cell activation, oxidative stress changes and upregulation of proinflammatory cytokine signaling. The great number of variable pathways, with several mediators interacting with each other, leads to a high number of candidates for potential therapeutic intervention. As far as surgical approaches are concerned, the modification of existing clamping techniques and the ischemic preconditioning are the most promising techniques till recently. In the search for novel techniques of protecting against hepatic ischemia reperfusion injury, many different strategies have been used in experimental models. The biggest part of this research lies around antioxidant therapy, but other potential solutions have been explored as well.ConclusionsThe management of hepatic trauma, in spite of the fact that it has become increasingly nonoperative, there still remains the possibility of hepatic resection in the hepatic trauma setting, especially in severe injuries. Hence, clinicians should be familiar with the concept of hepatic ischemia-reperfusion injury and respond appropriately and timely.

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“…Recently, compelling evidence has delineated the role of DCs in hepatic I/R injury and several results support that DCs modulate levels of IL-6 and IL-10 in liver submitted to ischemia injury ( 102 , 103 ). T lymphocytes (CD4+) produce chemokines that amplify KC activation, which promote neutrophil recruitment and adherence into the liver sinusoids, aggravating IR injury ( 104 ). CD4+ T cells accumulate rapidly in mouse LT following cold storage, and in this sense, as early as at 1 h post-transplant, a massive infiltration of liver graft with CD4 T cells is found.…”

Section: Discussionmentioning

confidence: 99%

NO–IL-6/10–IL-1β axis: a new pathway in steatotic and non-steatotic liver grafts from brain-dead donor rats

Casillas-Ramírez,

Micó-Carnero,

Sánchez-González

et al. 2023

Front. Immunol.

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IntroductionBrain death (BD) and steatosis are both risk factors for organ dysfunction or failure in liver transplantation (LT)Material and methodsHere, we examine the role of interleukin 6 (IL- 6) and IL-10 in LT of both non-steatotic and steatotic liver recovered from donors after brain death (DBDs), as well as the molecular signaling pathways underlying the effects of such cytokines.ResultsBD reduced IL-6 levels only in nonsteatotic grafts, and diminished IL-10 levels only in steatotic ones. In both graft types, BD increased IL-1β, which was associated with hepatic inflammation and damage. IL-6 administration reduced IL-1β only in non-steatotic grafts and protected them against damage and inflammation. Concordantly, IL-1β inhibition via treatment with an IL-1 receptor antagonist caused the same benefits in non-steatotic grafts. Treatment with IL-10 decreased IL-1β only in steatotic grafts and reduced injury and inflammation specifically in this graft type. Blockading the IL-1β effects also reduced damage and inflammation in steatotic grafts. Also, blockade of IL-1β action diminished hepatic cAMP in both types of livers, and this was associated with a reduction in liver injury and inflammation, then pointing to IL-1β regulating cAMP generation under LT and BD conditions. Additionally, the involvement of nitric oxide (NO) in the effects of interleukins was evaluated. Pharmacological inhibition of NO in LT from DBDs prompted even more evident reductions of IL-6 or IL-10 in non-steatotic and steatotic grafts, respectively. This exacerbated the already high levels of IL-1β seen in LT from DBDs, causing worse damage and inflammation in both graft types. The administration of NO donors to non-steatotic grafts potentiated the beneficial effects of endogenous NO, since it increased IL-6 levels, and reduced IL-1β, inflammation, and damage. However, treatment with NO donors in steatotic grafts did not modify IL-10 or IL-1β levels, but induced more injurious effects tan the induction of BD alone, characterized by increased nitrotyrosine, lipid peroxidation, inflammation, and hepatic damage.ConclusionOur study thus highlights the specificity of new signaling pathways in LT from DBDs: NO–IL-6–IL-1β in non-steatotic livers and NO–IL-10–IL-1β in steatotic ones. This opens up new therapeutic targets that could be useful in clinical LT.

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Ischemia-Reperfusion Injury Associated with Liver Transplantation in 2011: Past and Future

Cited by 4 publications

References 152 publications

Protective effects of St. John’s wort in the hepatic ischemia/reperfusion injury in rats

Protective effects of St. John’s wort in the hepatic ischemia/reperfusion injury in rats

Hepatic Ischemia and Reperfusion Injury and Trauma: Current Concepts

NO–IL-6/10–IL-1β axis: a new pathway in steatotic and non-steatotic liver grafts from brain-dead donor rats

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