TWEAK and LTß Signaling during Chronic Liver Disease
Chronic liver diseases (CLD) such as hepatitis B and C virus infection, alcoholic liver disease, and non-alcoholic steatohepatitis are associated with hepatocellular necrosis, continual inflammation, and hepatic fibrosis. The induced microenvironment triggers the activation of liver-resident progeni...
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| Format: | Journal Article |
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Frontiers Research Foundation
2014
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| Online Access: | http://hdl.handle.net/20.500.11937/4702 |
| _version_ | 1848744590329249792 |
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| author | Dwyer, Benjamin Olynyk, John Ramm, G. Tirnitz-Parker, Nina |
| author_facet | Dwyer, Benjamin Olynyk, John Ramm, G. Tirnitz-Parker, Nina |
| author_sort | Dwyer, Benjamin |
| building | Curtin Institutional Repository |
| collection | Online Access |
| description | Chronic liver diseases (CLD) such as hepatitis B and C virus infection, alcoholic liver disease, and non-alcoholic steatohepatitis are associated with hepatocellular necrosis, continual inflammation, and hepatic fibrosis. The induced microenvironment triggers the activation of liver-resident progenitor cells (LPCs) while hepatocyte replication is inhibited. In the early injury stages, LPCs regenerate the liver by proliferation, migration to sites of injury, and differentiation into functional biliary epithelial cells or hepatocytes. However, when this process becomes dysregulated, wound healing can progress to pathological fibrosis, cirrhosis, and eventually hepatocellular carcinoma. The other key mediators in the pathogenesis of progressive CLD are fibrosis-driving, activated hepatic stellate cells (HSCs) that usually proliferate in very close spatial association with LPCs. Recent studies from our group and others have suggested the potential for cytokine and chemokine cross-talk between LPCs and HSCs, which is mainly driven by the tumor necrosis factor (TNF) family members, TNF-like weak inducer of apoptosis (TWEAK) and lymphotoxin-β, potentially dictating the pathological outcomes of chronic liver injury. |
| first_indexed | 2025-11-14T06:03:53Z |
| format | Journal Article |
| id | curtin-20.500.11937-4702 |
| institution | Curtin University Malaysia |
| institution_category | Local University |
| last_indexed | 2025-11-14T06:03:53Z |
| publishDate | 2014 |
| publisher | Frontiers Research Foundation |
| recordtype | eprints |
| repository_type | Digital Repository |
| spelling | curtin-20.500.11937-47022019-02-19T04:26:13Z TWEAK and LTß Signaling during Chronic Liver Disease Dwyer, Benjamin Olynyk, John Ramm, G. Tirnitz-Parker, Nina regeneration TWEAK NFκB fibrosis LTβ liver progenitor cells cancer hepatic stellate cells Chronic liver diseases (CLD) such as hepatitis B and C virus infection, alcoholic liver disease, and non-alcoholic steatohepatitis are associated with hepatocellular necrosis, continual inflammation, and hepatic fibrosis. The induced microenvironment triggers the activation of liver-resident progenitor cells (LPCs) while hepatocyte replication is inhibited. In the early injury stages, LPCs regenerate the liver by proliferation, migration to sites of injury, and differentiation into functional biliary epithelial cells or hepatocytes. However, when this process becomes dysregulated, wound healing can progress to pathological fibrosis, cirrhosis, and eventually hepatocellular carcinoma. The other key mediators in the pathogenesis of progressive CLD are fibrosis-driving, activated hepatic stellate cells (HSCs) that usually proliferate in very close spatial association with LPCs. Recent studies from our group and others have suggested the potential for cytokine and chemokine cross-talk between LPCs and HSCs, which is mainly driven by the tumor necrosis factor (TNF) family members, TNF-like weak inducer of apoptosis (TWEAK) and lymphotoxin-β, potentially dictating the pathological outcomes of chronic liver injury. 2014 Journal Article http://hdl.handle.net/20.500.11937/4702 10.3389/fimmu.2014.00039 Frontiers Research Foundation fulltext |
| spellingShingle | regeneration TWEAK NFκB fibrosis LTβ liver progenitor cells cancer hepatic stellate cells Dwyer, Benjamin Olynyk, John Ramm, G. Tirnitz-Parker, Nina TWEAK and LTß Signaling during Chronic Liver Disease |
| title | TWEAK and LTß Signaling during Chronic Liver Disease |
| title_full | TWEAK and LTß Signaling during Chronic Liver Disease |
| title_fullStr | TWEAK and LTß Signaling during Chronic Liver Disease |
| title_full_unstemmed | TWEAK and LTß Signaling during Chronic Liver Disease |
| title_short | TWEAK and LTß Signaling during Chronic Liver Disease |
| title_sort | tweak and ltß signaling during chronic liver disease |
| topic | regeneration TWEAK NFκB fibrosis LTβ liver progenitor cells cancer hepatic stellate cells |
| url | http://hdl.handle.net/20.500.11937/4702 |