| Cellular basis of hepatic fibrosis and its role in inflammation and cancer . | |
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MedLine Citation:
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PMID: 23277047 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Multiple etiologies of liver injury can lead to fibrosis, which results from an imbalance between production and resorption of extracellular matrix. Hepatic stellate cells (HSCs), resident vitamin A storing cells, play a vital role in the response to injury. Upon activation, HSCs orchestrate the responsiveness of the liver to different types of injury, leading to deposition of excessive scar matrix into the interstitium as a wound-healing response. Quantitatively and qualitatively, the altered extracellular matrix (ECM) provides a permissive milieu for the development of cellular dysplasia and ultimately hepatocellular carcinoma (HCC). There is a range of underlying mechanisms that contribute to progression of fibrosis to HCC. As the functional complexity of HSC activation and its roles in inflammation, immune responses, angiogenesis, and proliferation are being clarified, new advances in therapeutic options for patients with chronic liver disease are emerging. |
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Authors:
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Peri Kocabayoglu; Scott L Friedman |
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Publication Detail:
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Type: Journal Article Date: 2013-01-01 |
Journal Detail:
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Title: Frontiers in bioscience (Scholar edition) Volume: 5 ISSN: 1945-0524 ISO Abbreviation: Front Biosci (Schol Ed) Publication Date: 2013 |
Date Detail:
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Created Date: 2013-01-01 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101485241 Medline TA: Front Biosci (Schol Ed) Country: United States |
Other Details:
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Languages: eng Pagination: 217-30 Citation Subset: IM |
Affiliation:
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Box 1123, Mount Sinai School of Medicine, 1425 Madison Ave., Room 1170C, New York, NY 10029, USA. |
Export Citation:
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Descriptor/Qualifier:
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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