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Research progress of natural compounds in anti-liver fibrosis by affecting autophagy of hepatic stellate cells
Chronic liver diseases caused by various pathogenesis are marked by inflammatory infiltration and wound healing reaction, while their normal regeneration ability is impaired. The unbalance between the generation and the degradation of extracellular matrix (ECM) leads to collagen accumulation and dev...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer Netherlands
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7925445/ https://www.ncbi.nlm.nih.gov/pubmed/33609264 http://dx.doi.org/10.1007/s11033-021-06171-w |
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author | Shu, Yongxiang Liu, Xuyou Huang, Haifeng Wen, Qi Shu, Jianchang |
author_facet | Shu, Yongxiang Liu, Xuyou Huang, Haifeng Wen, Qi Shu, Jianchang |
author_sort | Shu, Yongxiang |
collection | PubMed |
description | Chronic liver diseases caused by various pathogenesis are marked by inflammatory infiltration and wound healing reaction, while their normal regeneration ability is impaired. The unbalance between the generation and the degradation of extracellular matrix (ECM) leads to collagen accumulation and develops into liver fibrosis. Inflammation, oxidative stress, and autophagy interact closely in the pathogenesis of hepatic fibrosis. Reactive Oxygen Species (ROS) can not only stimulate Kupffer cells to release massive inflammatory factors, but induce autophagy. However, the latter may suppress inflammatory reaction by inhibiting proinflammatory complex formation directly, and removing damaged organelles or pathogenic microorganism indirectly. At present, effective anti-fibrosis drugs are still lacking. Previous studies have found various natural compounds enabled liver protection through anti-inflammatory, antioxidant, and other mechanisms. In recent years, autophagy, a vital life activity, has been found to be involved in the mechanism of liver fibrosis. As a new target, developing anti-liver fibrosis drugs that regulate the activity of autophagy is very promising. In this review, we summarize the latest studies about natural compounds in the treatment of liver fibrosis by regulating autophagy. |
format | Online Article Text |
id | pubmed-7925445 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Springer Netherlands |
record_format | MEDLINE/PubMed |
spelling | pubmed-79254452021-03-19 Research progress of natural compounds in anti-liver fibrosis by affecting autophagy of hepatic stellate cells Shu, Yongxiang Liu, Xuyou Huang, Haifeng Wen, Qi Shu, Jianchang Mol Biol Rep Mini Review Article Chronic liver diseases caused by various pathogenesis are marked by inflammatory infiltration and wound healing reaction, while their normal regeneration ability is impaired. The unbalance between the generation and the degradation of extracellular matrix (ECM) leads to collagen accumulation and develops into liver fibrosis. Inflammation, oxidative stress, and autophagy interact closely in the pathogenesis of hepatic fibrosis. Reactive Oxygen Species (ROS) can not only stimulate Kupffer cells to release massive inflammatory factors, but induce autophagy. However, the latter may suppress inflammatory reaction by inhibiting proinflammatory complex formation directly, and removing damaged organelles or pathogenic microorganism indirectly. At present, effective anti-fibrosis drugs are still lacking. Previous studies have found various natural compounds enabled liver protection through anti-inflammatory, antioxidant, and other mechanisms. In recent years, autophagy, a vital life activity, has been found to be involved in the mechanism of liver fibrosis. As a new target, developing anti-liver fibrosis drugs that regulate the activity of autophagy is very promising. In this review, we summarize the latest studies about natural compounds in the treatment of liver fibrosis by regulating autophagy. Springer Netherlands 2021-02-20 2021 /pmc/articles/PMC7925445/ /pubmed/33609264 http://dx.doi.org/10.1007/s11033-021-06171-w Text en © The Author(s) 2021 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Mini Review Article Shu, Yongxiang Liu, Xuyou Huang, Haifeng Wen, Qi Shu, Jianchang Research progress of natural compounds in anti-liver fibrosis by affecting autophagy of hepatic stellate cells |
title | Research progress of natural compounds in anti-liver fibrosis by affecting autophagy of hepatic stellate cells |
title_full | Research progress of natural compounds in anti-liver fibrosis by affecting autophagy of hepatic stellate cells |
title_fullStr | Research progress of natural compounds in anti-liver fibrosis by affecting autophagy of hepatic stellate cells |
title_full_unstemmed | Research progress of natural compounds in anti-liver fibrosis by affecting autophagy of hepatic stellate cells |
title_short | Research progress of natural compounds in anti-liver fibrosis by affecting autophagy of hepatic stellate cells |
title_sort | research progress of natural compounds in anti-liver fibrosis by affecting autophagy of hepatic stellate cells |
topic | Mini Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7925445/ https://www.ncbi.nlm.nih.gov/pubmed/33609264 http://dx.doi.org/10.1007/s11033-021-06171-w |
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