The response of the hepatocyte to ischemia

Massip-Salcedo, Marta; Roselló-Catafau, J.; Prieto, Jesús; Ávila, Matías A.; Peralta, Carmen

doi:10.1111/j.1478-3231.2006.01390.x

Cited by 97 publications

(125 citation statements)

References 111 publications

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“…The activation of caspases has also been used to demonstrate apoptosis in rat SECs following cold IRI (39). On the other hand, newer studies oppose the view that most cells undergo apoptosis in response to either warm or cold IRI, believing that necrosis is the principle form of cell death (12). The events that occur during the anoxia and the different phases of the reperfusion injury are being summarized in Table 1.…”

Section: Apoptosis and Necrosismentioning

confidence: 99%

“…More specifically, a decrease in oxidative phosphorylation, results in Adenosine-5'-triphosphate (ATP) depletion and derangements in calcium homeostasis (11). The lack of oxygen to hepatocytes during ischemia also causes mitochondrial deenergization, alterations of H + and Na + homeostasis, and finally swelling of the sinusoidal endothelial cells (SEC), and the KC (12). Activation of KC with production of reactive oxygen species (ROS), upregulation of the inducible nitric oxide synthase (iNOS) in hepatocytes, and upregulation of proinflammatory cytokines, chemokines, and adhesion molecules resulting in neutrophil-mediated injury, are all major contributing events to the inflammation-associated damage (13).…”

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

confidence: 99%

See 1 more Smart Citation

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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Section: Apoptosis and Necrosismentioning

confidence: 99%

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

confidence: 99%

Hepatic Ischemia and Reperfusion Injury and Trauma: Current Concepts

Papadopoulos¹,

Siempis²,

Theodorakou³

et al. 2013

Arch Trauma Res

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“…Hepatocyte necrosis is present not only during ischemia but also during reperfusion (16). Oxidative stress and reactive oxygen species (ROS) may lead to injury either directly, by oxidation of proteins, lipids or DNA, or indirectly, by inflammatory cascade initiation and hepatocytes changes (17).…”

Section: Pathophysiologymentioning

confidence: 99%

Ischemic Hepatitis – Intercorrelated Pathology

Ciobanu

Gherasim

2018

Maedica

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“…During ischemia reperfusion injury, generation of reactive oxygen species (ROS) is carried out. These species may interact with essential cellular targets, including proteins, lipids and DNA, compromising cell viability and function (3,4). However, liver cells, mainly hepatocytes have developed a comprehensive array of antioxidant defenses to prevent formation of ROS or limit their damaging effects.…”

Section: Introductionmentioning

confidence: 99%