Liver Fibrosis and Altered Matrix Synthesis
Liver fibrosis represents the uniform response of liver to toxic, infectious or metabolic agents. The process leading to liver fibrosis resembles the process of wound healing, including the three phases following tissue injury: inflammation, synthesis of collagenous and noncollagenous extracellular...
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| Format: | Article |
| Language: | English |
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Wiley
2001-01-01
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| Series: | Canadian Journal of Gastroenterology |
| Online Access: | http://dx.doi.org/10.1155/2001/870205 |
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| _version_ | 1832551135235276800 |
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| author | Katrin Neubauer Bernhard Saile Giuliano Ramadori |
| author_facet | Katrin Neubauer Bernhard Saile Giuliano Ramadori |
| author_sort | Katrin Neubauer |
| collection | DOAJ |
| description | Liver fibrosis represents the uniform response of liver to toxic, infectious or metabolic agents. The process leading to liver fibrosis resembles the process of wound healing, including the three phases following tissue injury: inflammation, synthesis of collagenous and noncollagenous extracellular matrix components, and tissue remodelling (scar formation). While a single liver tissue injury can be followed by an almost complete restitution ad integrum, the persistence of the original damaging noxa results in tissue damage. During the establishment of liver fibrosis, the basement membrane components collagen type IV, entactin and laminin increase and form a basement membrane-like structure within the space of Disse. The number of endothelial fenestrae of the sinusoids decreases. These changes of the sinusoids are called 'capillarization' because the altered structure of the sinusoids resembles that of capillaries. At the cellular level, origin of liver fibrogenesis is initiated by the damage of hepatocytes, resulting in the recruitment of inflammatory cells and platelets, and activation of Kupffer cells, with subsequent release of cytokines and growth factors. The hepatic stellate cells seem to be the primary target cells for these inflammatory stimuli, because during fibrogenesis, they undergo an activation process to a myofibroblast-like cell, which represents the major matrix-producing cell. Based on this pathophysiological mechanism, therapeutic methods are developed to inhibit matrix synthesis or stimulate matrix degradation. A number of substances are currently being tested that either neutralize fibrogenic stimuli and prevent the activation of hepatic stellate cells, or directly modulate the matrix metabolism. However, until now, the elimination of the hepatotoxins has been the sole therapeutic concept available for the treatment of liver fibrogenesis in humans. |
| format | Article |
| id | doaj-art-aaf7d31ee3534a9897336066d8e24816 |
| institution | Kabale University |
| issn | 0835-7900 |
| language | English |
| publishDate | 2001-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Canadian Journal of Gastroenterology |
| spelling | doaj-art-aaf7d31ee3534a9897336066d8e248162025-02-03T06:04:57ZengWileyCanadian Journal of Gastroenterology0835-79002001-01-0115318719310.1155/2001/870205Liver Fibrosis and Altered Matrix SynthesisKatrin Neubauer0Bernhard Saile1Giuliano Ramadori2University of Göttingen, Department of Internal Medicine, Section of Gastroenterology and Endocrinology, Göttingen, GermanyUniversity of Göttingen, Department of Internal Medicine, Section of Gastroenterology and Endocrinology, Göttingen, GermanyUniversity of Göttingen, Department of Internal Medicine, Section of Gastroenterology and Endocrinology, Göttingen, GermanyLiver fibrosis represents the uniform response of liver to toxic, infectious or metabolic agents. The process leading to liver fibrosis resembles the process of wound healing, including the three phases following tissue injury: inflammation, synthesis of collagenous and noncollagenous extracellular matrix components, and tissue remodelling (scar formation). While a single liver tissue injury can be followed by an almost complete restitution ad integrum, the persistence of the original damaging noxa results in tissue damage. During the establishment of liver fibrosis, the basement membrane components collagen type IV, entactin and laminin increase and form a basement membrane-like structure within the space of Disse. The number of endothelial fenestrae of the sinusoids decreases. These changes of the sinusoids are called 'capillarization' because the altered structure of the sinusoids resembles that of capillaries. At the cellular level, origin of liver fibrogenesis is initiated by the damage of hepatocytes, resulting in the recruitment of inflammatory cells and platelets, and activation of Kupffer cells, with subsequent release of cytokines and growth factors. The hepatic stellate cells seem to be the primary target cells for these inflammatory stimuli, because during fibrogenesis, they undergo an activation process to a myofibroblast-like cell, which represents the major matrix-producing cell. Based on this pathophysiological mechanism, therapeutic methods are developed to inhibit matrix synthesis or stimulate matrix degradation. A number of substances are currently being tested that either neutralize fibrogenic stimuli and prevent the activation of hepatic stellate cells, or directly modulate the matrix metabolism. However, until now, the elimination of the hepatotoxins has been the sole therapeutic concept available for the treatment of liver fibrogenesis in humans.http://dx.doi.org/10.1155/2001/870205 |
| spellingShingle | Katrin Neubauer Bernhard Saile Giuliano Ramadori Liver Fibrosis and Altered Matrix Synthesis Canadian Journal of Gastroenterology |
| title | Liver Fibrosis and Altered Matrix Synthesis |
| title_full | Liver Fibrosis and Altered Matrix Synthesis |
| title_fullStr | Liver Fibrosis and Altered Matrix Synthesis |
| title_full_unstemmed | Liver Fibrosis and Altered Matrix Synthesis |
| title_short | Liver Fibrosis and Altered Matrix Synthesis |
| title_sort | liver fibrosis and altered matrix synthesis |
| url | http://dx.doi.org/10.1155/2001/870205 |
| work_keys_str_mv | AT katrinneubauer liverfibrosisandalteredmatrixsynthesis AT bernhardsaile liverfibrosisandalteredmatrixsynthesis AT giulianoramadori liverfibrosisandalteredmatrixsynthesis |