Role of Angiopoietin/Tie2 in Critical Illness: Promising Biomarker, Disease Mediator, and Therapeutic Target?
Critical illness is a descriptive, broad term for a serious clinical condition that can result from enormously heterogeneous etiologies. A common end feature these patients regularly suffer from is the so-called multiple organ dysfunction syndrome (MODS), often a consequence of organ hypoperfusion a...
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Wiley
2012-01-01
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| Series: | Scientifica |
| Online Access: | http://dx.doi.org/10.6064/2012/160174 |
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| author | Alexander Lukasz Philipp Kümpers Sascha David |
| author_facet | Alexander Lukasz Philipp Kümpers Sascha David |
| author_sort | Alexander Lukasz |
| collection | DOAJ |
| description | Critical illness is a descriptive, broad term for a serious clinical condition that can result from enormously heterogeneous etiologies. A common end feature these patients regularly suffer from is the so-called multiple organ dysfunction syndrome (MODS), often a consequence of organ hypoperfusion and ischemia, coagulopathies, overwhelming inflammatory responses, immune paralysis and mitochondrial dysfunction. Mechanistically, endothelial injury and particularly microvascular leakage is a major step in the pathophysiology of MODS and contributes to its mortality.
The angiopoietin (Angpt)/Tie2 system consists of the endothelial tyrosine kinase Tie2 and its 4 circulating ligands (Angpt1-4). The balance between the agonistic ligand “Angpt-1" and the antagonistic one “Angpt-2" regulates baseline endothelial barrier function and its response to injury and is therefore considered a gatekeeper of endothelial activation.
This paper provides a systematic overview of the Angpt/Tie2 system with respect to (1) its role as a global biomarker of endothelial activation in critical ill patients, (2) its contribution to MODS pathophysiology as a disease mediator, and last but not least (3) putative therapeutic applications to modify the activation state of Tie2 in mice and men. |
| format | Article |
| id | doaj-art-ea86a32ae0d5466596e72af2e2405211 |
| institution | OA Journals |
| issn | 2090-908X |
| language | English |
| publishDate | 2012-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Scientifica |
| spelling | doaj-art-ea86a32ae0d5466596e72af2e24052112025-08-20T02:22:02ZengWileyScientifica2090-908X2012-01-01201210.6064/2012/160174160174Role of Angiopoietin/Tie2 in Critical Illness: Promising Biomarker, Disease Mediator, and Therapeutic Target?Alexander Lukasz0Philipp Kümpers1Sascha David2Department of Nephrology & Hypertension, Hannover Medical School, Carl-Neuberg Straße 1, 30625 Hannover, GermanyDepartment of Internal Medicine, Rheumatology and Nephrology, University Hospital Münster, 48149Münster, GermanyDepartment of Nephrology & Hypertension, Hannover Medical School, Carl-Neuberg Straße 1, 30625 Hannover, GermanyCritical illness is a descriptive, broad term for a serious clinical condition that can result from enormously heterogeneous etiologies. A common end feature these patients regularly suffer from is the so-called multiple organ dysfunction syndrome (MODS), often a consequence of organ hypoperfusion and ischemia, coagulopathies, overwhelming inflammatory responses, immune paralysis and mitochondrial dysfunction. Mechanistically, endothelial injury and particularly microvascular leakage is a major step in the pathophysiology of MODS and contributes to its mortality. The angiopoietin (Angpt)/Tie2 system consists of the endothelial tyrosine kinase Tie2 and its 4 circulating ligands (Angpt1-4). The balance between the agonistic ligand “Angpt-1" and the antagonistic one “Angpt-2" regulates baseline endothelial barrier function and its response to injury and is therefore considered a gatekeeper of endothelial activation. This paper provides a systematic overview of the Angpt/Tie2 system with respect to (1) its role as a global biomarker of endothelial activation in critical ill patients, (2) its contribution to MODS pathophysiology as a disease mediator, and last but not least (3) putative therapeutic applications to modify the activation state of Tie2 in mice and men.http://dx.doi.org/10.6064/2012/160174 |
| spellingShingle | Alexander Lukasz Philipp Kümpers Sascha David Role of Angiopoietin/Tie2 in Critical Illness: Promising Biomarker, Disease Mediator, and Therapeutic Target? Scientifica |
| title | Role of Angiopoietin/Tie2 in Critical Illness: Promising Biomarker, Disease Mediator, and Therapeutic Target? |
| title_full | Role of Angiopoietin/Tie2 in Critical Illness: Promising Biomarker, Disease Mediator, and Therapeutic Target? |
| title_fullStr | Role of Angiopoietin/Tie2 in Critical Illness: Promising Biomarker, Disease Mediator, and Therapeutic Target? |
| title_full_unstemmed | Role of Angiopoietin/Tie2 in Critical Illness: Promising Biomarker, Disease Mediator, and Therapeutic Target? |
| title_short | Role of Angiopoietin/Tie2 in Critical Illness: Promising Biomarker, Disease Mediator, and Therapeutic Target? |
| title_sort | role of angiopoietin tie2 in critical illness promising biomarker disease mediator and therapeutic target |
| url | http://dx.doi.org/10.6064/2012/160174 |
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