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Ischemia/Reperfusion injury in liver surgery and transplantation: pathophysiology.

Weigand K, Brost S, Steinebrunner N, Büchler M, Schemmer P, Müller M - HPB Surg (2012)

Bottom Line: Liver ischemia/reperfusion (IR) injury is caused by a heavily toothed network of interactions of cells of the immune system, cytokine production, and reduced microcirculatory blood flow in the liver.These complex networks are further elaborated by multiple intracellular pathways activated by cytokines, chemokines, and danger-associated molecular patterns.Overall, enhanced production of reactive oxygen species, found very early in IR injury, plays an important role in liver tissue damage at several points within these complex networks.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, Endocrinology, Rheumatology and Infectious Diseases, University Hospital Regensburg, D-93053 Regensburg, Germany.

ABSTRACT
Liver ischemia/reperfusion (IR) injury is caused by a heavily toothed network of interactions of cells of the immune system, cytokine production, and reduced microcirculatory blood flow in the liver. These complex networks are further elaborated by multiple intracellular pathways activated by cytokines, chemokines, and danger-associated molecular patterns. Furthermore, intracellular ionic disturbances and especially mitochondrial disorders play an important role leading to apoptosis and necrosis of hepatocytes in IR injury. Overall, enhanced production of reactive oxygen species, found very early in IR injury, plays an important role in liver tissue damage at several points within these complex networks. Many contributors to IR injury are only incompletely understood so far. This paper tempts to give an overview of the different mechanisms involved in the formation of IR injury. Only by further elucidation of these complex mechanisms IR injury can be understood and possible therapeutic strategies can be improved or be developed.

No MeSH data available.


Related in: MedlinePlus

Cellular interaction involved in IR injury, resulting in cellular swelling, apoptosis, and necrosis. ATP: adenosine triphosphate; ICAM-1: intercellular adhesion molecule-1; KC: Kupffer cell; IL-1, interleukin-1; NKT: natural killer T cell; NO: nitric oxide; ROS: reactive oxygen species; SEC: sinusoidal endothelial cells; T cell: CD4+ T lymphocyte; TNF: tumor necrosis factor; VCAM-1: vascular adhesion molecule-1.
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Related In: Results  -  Collection


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fig2: Cellular interaction involved in IR injury, resulting in cellular swelling, apoptosis, and necrosis. ATP: adenosine triphosphate; ICAM-1: intercellular adhesion molecule-1; KC: Kupffer cell; IL-1, interleukin-1; NKT: natural killer T cell; NO: nitric oxide; ROS: reactive oxygen species; SEC: sinusoidal endothelial cells; T cell: CD4+ T lymphocyte; TNF: tumor necrosis factor; VCAM-1: vascular adhesion molecule-1.

Mentions: The expressed cell-surface adhesion molecules on hepatocytes and SEC include intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1) [28, 73]. Neutrophils bind to ICAM-1 and VCAM-1 and by doing so migrate across the endothelium into the liver parenchyma enhancing ROS production and degranulation of cytoplasmic vesicles containing enzymes capable to degrade extracellular matrix and hepatocytes [28] (Figure 2).


Ischemia/Reperfusion injury in liver surgery and transplantation: pathophysiology.

Weigand K, Brost S, Steinebrunner N, Büchler M, Schemmer P, Müller M - HPB Surg (2012)

Cellular interaction involved in IR injury, resulting in cellular swelling, apoptosis, and necrosis. ATP: adenosine triphosphate; ICAM-1: intercellular adhesion molecule-1; KC: Kupffer cell; IL-1, interleukin-1; NKT: natural killer T cell; NO: nitric oxide; ROS: reactive oxygen species; SEC: sinusoidal endothelial cells; T cell: CD4+ T lymphocyte; TNF: tumor necrosis factor; VCAM-1: vascular adhesion molecule-1.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3369424&req=5

fig2: Cellular interaction involved in IR injury, resulting in cellular swelling, apoptosis, and necrosis. ATP: adenosine triphosphate; ICAM-1: intercellular adhesion molecule-1; KC: Kupffer cell; IL-1, interleukin-1; NKT: natural killer T cell; NO: nitric oxide; ROS: reactive oxygen species; SEC: sinusoidal endothelial cells; T cell: CD4+ T lymphocyte; TNF: tumor necrosis factor; VCAM-1: vascular adhesion molecule-1.
Mentions: The expressed cell-surface adhesion molecules on hepatocytes and SEC include intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1) [28, 73]. Neutrophils bind to ICAM-1 and VCAM-1 and by doing so migrate across the endothelium into the liver parenchyma enhancing ROS production and degranulation of cytoplasmic vesicles containing enzymes capable to degrade extracellular matrix and hepatocytes [28] (Figure 2).

Bottom Line: Liver ischemia/reperfusion (IR) injury is caused by a heavily toothed network of interactions of cells of the immune system, cytokine production, and reduced microcirculatory blood flow in the liver.These complex networks are further elaborated by multiple intracellular pathways activated by cytokines, chemokines, and danger-associated molecular patterns.Overall, enhanced production of reactive oxygen species, found very early in IR injury, plays an important role in liver tissue damage at several points within these complex networks.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, Endocrinology, Rheumatology and Infectious Diseases, University Hospital Regensburg, D-93053 Regensburg, Germany.

ABSTRACT
Liver ischemia/reperfusion (IR) injury is caused by a heavily toothed network of interactions of cells of the immune system, cytokine production, and reduced microcirculatory blood flow in the liver. These complex networks are further elaborated by multiple intracellular pathways activated by cytokines, chemokines, and danger-associated molecular patterns. Furthermore, intracellular ionic disturbances and especially mitochondrial disorders play an important role leading to apoptosis and necrosis of hepatocytes in IR injury. Overall, enhanced production of reactive oxygen species, found very early in IR injury, plays an important role in liver tissue damage at several points within these complex networks. Many contributors to IR injury are only incompletely understood so far. This paper tempts to give an overview of the different mechanisms involved in the formation of IR injury. Only by further elucidation of these complex mechanisms IR injury can be understood and possible therapeutic strategies can be improved or be developed.

No MeSH data available.


Related in: MedlinePlus