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Autophagy in Hepatic Fibrosis
Hepatic fibrosis is a leading cause of morbidity and mortality worldwide. Hepatic fibrosis is usually associated with chronic liver diseases caused by infection, drugs, metabolic disorders, or autoimmune imbalances. Effective clinical therapies are still lacking. Autophagy is a cellular process that...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3980865/ https://www.ncbi.nlm.nih.gov/pubmed/24779010 http://dx.doi.org/10.1155/2014/436242 |
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author | Song, Yang Zhao, Yingying Wang, Fei Tao, Lichan Xiao, Junjie Yang, Changqing |
author_facet | Song, Yang Zhao, Yingying Wang, Fei Tao, Lichan Xiao, Junjie Yang, Changqing |
author_sort | Song, Yang |
collection | PubMed |
description | Hepatic fibrosis is a leading cause of morbidity and mortality worldwide. Hepatic fibrosis is usually associated with chronic liver diseases caused by infection, drugs, metabolic disorders, or autoimmune imbalances. Effective clinical therapies are still lacking. Autophagy is a cellular process that degrades damaged organelles or protein aggregation, which participates in many pathological processes including liver diseases. Autophagy participates in hepatic fibrosis by activating hepatic stellate cells and may participate as well through influencing other fibrogenic cells. Besides that, autophagy can induce some liver diseases to develop while it may play a protective role in hepatocellular abnormal aggregates related liver diseases and reduces fibrosis. With a better understanding of the potential effects of autophagy on hepatic fibrosis, targeting autophagy might be a novel therapeutic strategy for hepatic fibrosis in the near future. |
format | Online Article Text |
id | pubmed-3980865 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-39808652014-04-28 Autophagy in Hepatic Fibrosis Song, Yang Zhao, Yingying Wang, Fei Tao, Lichan Xiao, Junjie Yang, Changqing Biomed Res Int Review Article Hepatic fibrosis is a leading cause of morbidity and mortality worldwide. Hepatic fibrosis is usually associated with chronic liver diseases caused by infection, drugs, metabolic disorders, or autoimmune imbalances. Effective clinical therapies are still lacking. Autophagy is a cellular process that degrades damaged organelles or protein aggregation, which participates in many pathological processes including liver diseases. Autophagy participates in hepatic fibrosis by activating hepatic stellate cells and may participate as well through influencing other fibrogenic cells. Besides that, autophagy can induce some liver diseases to develop while it may play a protective role in hepatocellular abnormal aggregates related liver diseases and reduces fibrosis. With a better understanding of the potential effects of autophagy on hepatic fibrosis, targeting autophagy might be a novel therapeutic strategy for hepatic fibrosis in the near future. Hindawi Publishing Corporation 2014 2014-03-23 /pmc/articles/PMC3980865/ /pubmed/24779010 http://dx.doi.org/10.1155/2014/436242 Text en Copyright © 2014 Yang Song et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Song, Yang Zhao, Yingying Wang, Fei Tao, Lichan Xiao, Junjie Yang, Changqing Autophagy in Hepatic Fibrosis |
title | Autophagy in Hepatic Fibrosis |
title_full | Autophagy in Hepatic Fibrosis |
title_fullStr | Autophagy in Hepatic Fibrosis |
title_full_unstemmed | Autophagy in Hepatic Fibrosis |
title_short | Autophagy in Hepatic Fibrosis |
title_sort | autophagy in hepatic fibrosis |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3980865/ https://www.ncbi.nlm.nih.gov/pubmed/24779010 http://dx.doi.org/10.1155/2014/436242 |
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