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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

Intracellular signalling pathways and ionic disturbances engaged during IR injury, resulting in cellular swelling, apoptosis, and necrosis. ADP: adenosine diphosphate; AMP: adenosine monophosphate; AP-1: activator protein-1; ATP: adenosine triphosphate; DAMP: danger-associated molecular pattern; HMGB-1: high mobility group box-1; ICAM-1: intercellular adhesion molecule-1; IL-1: interleukin-1; JNK: c-Jun N-terminal kinase; MAPK: mitogen-activated protein kinase; MPT pore: mitochondrial permeability transition pore; MyD88: myeloid differentiation factor 88; NF-κB: nuclear factor kappa B; RAGE: receptor for advanced gylcation end product; ROS: reactive oxygen species; SOC: store operated calcium channel; TLR: toll-like receptor; TNF: tumor necrosis factor; TRAM: TRIF-related adaptor molecule; TRIF: TIR domain-containing adaptor inducing interferon; TRP: transient receptor protein; VCAM-1: vascular adhesion molecule-1.
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Related In: Results  -  Collection


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fig1: Intracellular signalling pathways and ionic disturbances engaged during IR injury, resulting in cellular swelling, apoptosis, and necrosis. ADP: adenosine diphosphate; AMP: adenosine monophosphate; AP-1: activator protein-1; ATP: adenosine triphosphate; DAMP: danger-associated molecular pattern; HMGB-1: high mobility group box-1; ICAM-1: intercellular adhesion molecule-1; IL-1: interleukin-1; JNK: c-Jun N-terminal kinase; MAPK: mitogen-activated protein kinase; MPT pore: mitochondrial permeability transition pore; MyD88: myeloid differentiation factor 88; NF-κB: nuclear factor kappa B; RAGE: receptor for advanced gylcation end product; ROS: reactive oxygen species; SOC: store operated calcium channel; TLR: toll-like receptor; TNF: tumor necrosis factor; TRAM: TRIF-related adaptor molecule; TRIF: TIR domain-containing adaptor inducing interferon; TRP: transient receptor protein; VCAM-1: vascular adhesion molecule-1.

Mentions: Furthermore, this counteracts the protective effect of an acidic pH during reperfusion [57], for example, the maintenance of an acidic pH prevents the formation of MPT pores [49]. However, these regulations are still based on experimental observations and need to be studied further to understand the relevance in IR injury (Figure 1).


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

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

Intracellular signalling pathways and ionic disturbances engaged during IR injury, resulting in cellular swelling, apoptosis, and necrosis. ADP: adenosine diphosphate; AMP: adenosine monophosphate; AP-1: activator protein-1; ATP: adenosine triphosphate; DAMP: danger-associated molecular pattern; HMGB-1: high mobility group box-1; ICAM-1: intercellular adhesion molecule-1; IL-1: interleukin-1; JNK: c-Jun N-terminal kinase; MAPK: mitogen-activated protein kinase; MPT pore: mitochondrial permeability transition pore; MyD88: myeloid differentiation factor 88; NF-κB: nuclear factor kappa B; RAGE: receptor for advanced gylcation end product; ROS: reactive oxygen species; SOC: store operated calcium channel; TLR: toll-like receptor; TNF: tumor necrosis factor; TRAM: TRIF-related adaptor molecule; TRIF: TIR domain-containing adaptor inducing interferon; TRP: transient receptor protein; VCAM-1: vascular adhesion molecule-1.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig1: Intracellular signalling pathways and ionic disturbances engaged during IR injury, resulting in cellular swelling, apoptosis, and necrosis. ADP: adenosine diphosphate; AMP: adenosine monophosphate; AP-1: activator protein-1; ATP: adenosine triphosphate; DAMP: danger-associated molecular pattern; HMGB-1: high mobility group box-1; ICAM-1: intercellular adhesion molecule-1; IL-1: interleukin-1; JNK: c-Jun N-terminal kinase; MAPK: mitogen-activated protein kinase; MPT pore: mitochondrial permeability transition pore; MyD88: myeloid differentiation factor 88; NF-κB: nuclear factor kappa B; RAGE: receptor for advanced gylcation end product; ROS: reactive oxygen species; SOC: store operated calcium channel; TLR: toll-like receptor; TNF: tumor necrosis factor; TRAM: TRIF-related adaptor molecule; TRIF: TIR domain-containing adaptor inducing interferon; TRP: transient receptor protein; VCAM-1: vascular adhesion molecule-1.
Mentions: Furthermore, this counteracts the protective effect of an acidic pH during reperfusion [57], for example, the maintenance of an acidic pH prevents the formation of MPT pores [49]. However, these regulations are still based on experimental observations and need to be studied further to understand the relevance in IR injury (Figure 1).

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