Past and future approaches to ischemia-reperfusion lesion associated with liver transplantation

Casillas-Ramírez, Araní; Mosbah, Ismaïl Ben; Ramalho, Fernando Silva; Roselló‐Catafau, Joan; Peralta, Carmen

doi:10.1016/j.lfs.2006.06.024

Cited by 186 publications

(191 citation statements)

References 171 publications

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“…This is an important issue considering that pharmacological and other liver preconditioning maneuvers have not been transferred to clinical application, with the exception of ischemic preconditioning (91). Conversely, the usefulness of ischemic preconditioning in human liver resections (92)(93)(94) and in human liver transplantation (95-97) remains controversial (98)(99)(100).…”

Section: Discussionmentioning

confidence: 99%

Hormetic responses of thyroid hormone calorigenesis in the liver: Association with oxidative stress

Videla

2010

IUBMB Life

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SummaryThyroid hormone (L-3,3 0 ,5-triiodothyronine, T 3 ) exerts calorigenic effects by accelerating mitochondrial O 2 consumption through transcriptional activation of respiratory genes, with consequent increased reactive oxygen species (ROS) production. In the liver, ROS generation occurs at different sites of hepatocytes and in the respiratory burst of Kupffer cells, triggering the activation of the transcription factors nuclear factor-jB, signal transducer and activator of transcription 3, and activating protein 1. Under these conditions, the redox upregulation of Kupffer cell-dependent expression of cytokines [tumor necrosis factor-a, interleukin (IL)-1, and IL-6] is achieved, which upon interaction with specific receptors in hepatocytes trigger the expression of antioxidant enzymes (manganese superoxide dismutase, inducible nitric oxide synthase), antiapoptotic proteins (Bcl-2), and acute-phase proteins (haptoglobin, b-fibrinogen). These responses and the promotion of hepatocyte and Kupffer cell proliferation observed represent hormetic effects re-establishing redox homeostasis, promoting cell survival, and protecting the liver against ischemia-reperfusion (IR) injury. It is proposed that hormesis underlying T 3 action may constitute a novel preconditioning strategy for IR injury during liver surgery in man or in liver transplantation using reduced-size grafts from living donors, considering that (i) with the exception of the controversial ischemic preconditioning, all other studied strategies have failed to reach the clinical setting and (ii) T 3 is a well-tolerated therapeutic agent that either lacks major adverse effects or has minimal and controlled side effects. IUBMBIUBMB Life, 62(6): [460][461][462][463][464][465][466] 2010

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Section: Discussionmentioning

confidence: 99%

Hormetic responses of thyroid hormone calorigenesis in the liver: Association with oxidative stress

Videla

2010

IUBMB Life

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“…During an ischemic period, several functional changes occur at the cellular level that promote cell injury (10). More specifically, a decrease in oxidative phosphorylation, results in Adenosine-5'-triphosphate (ATP) depletion and derangements in calcium homeostasis (11).…”

Section: Current Knowledge Of the Pathophysiology Of Hepatic I/r Injurymentioning

confidence: 99%

“…The source of ROS in hepatic IRI has long been controversial. Regarding the mechanisms responsible for ROS production, experiments with xanthine oxidase (XOD)/xanthine dehydrogenase (XDH) inhibitors, such as allopurinol, suggest that the XOD/XDH system is the main ROS generator in hepatocytes (10). However, other results obtained in experimental models of the isolated perfused liver have suggested that the mitochondria, through the respiratory chain, could be the main source of ROS (17).…”

Section: Ros Creation Kupffer Cells and Chemokine Secretionmentioning

confidence: 99%

Hepatic Ischemia and Reperfusion Injury and Trauma: Current Concepts

Papadopoulos¹,

Siempis²,

Theodorakou³

et al. 2013

Arch Trauma Res

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Context: Ischemia-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 Acquisition: The 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. Results: The 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. Conclusions:The 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.Keywords: Reperfusion Injury; Ischemia; Pathophysiology; Prevention Implication for health policy/practice/research/medical education: Hepatic ischemia and reperfusion injury is a complex phenomenon which is commonplace in clinical practice such as the operative management of hepatic trauma, liver transplantation and liver resection. Hence, surgeons should be familiar with it and apply the necessary methods to prevent it.

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“…Summary of the mechanisms involved in hepatic ischemia-reperfusion injury. (Bilzer & Gerber, 2000;Casillas et al, 2006;Jaeschke, 1998Jaeschke, , 2003Lentsch et al, 2000;Massip-Salcedo et al, 2007 ;Peralta et al, 1996Peralta et al, , 2000a pathophysiological relevance of intracellular oxidant stress during reperfusion (Grattagliano et al, 1999;Metzger et al, 1988). Grattagliano et al, 1999, demonstrated that mitochondria do not seem to actively participate in the reperfusion-induced oxidative stress.…”

Section: Mechanisms Responsible For Ros Productionmentioning

confidence: 99%

“…2). , 2010;Casillas et al, 2006;Fernández et al, 2004;Ghobrial et al, 2005;Jaeschke &Lemasters, 2003;Malhi et al, 2006;Massip-Salcedo et al, 2007;Selzner et al, 2000;Yin, 2000) …”

Section: Cell Death In Liver Transplantationunclassified

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

Elias-Miró¹,

Jiménez‐Castro²,

Peralta³

2012

Liver Transplantation - Basic Issues

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Past and future approaches to ischemia-reperfusion lesion associated with liver transplantation

Cited by 186 publications

References 171 publications

Hormetic responses of thyroid hormone calorigenesis in the liver: Association with oxidative stress

Hormetic responses of thyroid hormone calorigenesis in the liver: Association with oxidative stress

Hepatic Ischemia and Reperfusion Injury and Trauma: Current Concepts

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

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