Cargando…
Animal and Organoid Models of Liver Fibrosis
Liver fibrosis refers to the process underlying the development of chronic liver diseases, wherein liver cells are repeatedly destroyed and regenerated, which leads to an excessive deposition and abnormal distribution of the extracellular matrix such as collagen, glycoprotein and proteoglycan in the...
Autores principales: | , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2021
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8187919/ https://www.ncbi.nlm.nih.gov/pubmed/34122138 http://dx.doi.org/10.3389/fphys.2021.666138 |
_version_ | 1783705235089260544 |
---|---|
author | Bao, Yu-long Wang, Li Pan, Hai-ting Zhang, Tai-ran Chen, Ya-hong Xu, Shan-jing Mao, Xin-li Li, Shao-wei |
author_facet | Bao, Yu-long Wang, Li Pan, Hai-ting Zhang, Tai-ran Chen, Ya-hong Xu, Shan-jing Mao, Xin-li Li, Shao-wei |
author_sort | Bao, Yu-long |
collection | PubMed |
description | Liver fibrosis refers to the process underlying the development of chronic liver diseases, wherein liver cells are repeatedly destroyed and regenerated, which leads to an excessive deposition and abnormal distribution of the extracellular matrix such as collagen, glycoprotein and proteoglycan in the liver. Liver fibrosis thus constitutes the pathological repair response of the liver to chronic injury. Hepatic fibrosis is a key step in the progression of chronic liver disease to cirrhosis and an important factor affecting the prognosis of chronic liver disease. Further development of liver fibrosis may lead to structural disorders of the liver, nodular regeneration of hepatocytes and the formation of cirrhosis. Hepatic fibrosis is histologically reversible if treated aggressively during this period, but when fibrosis progresses to the stage of cirrhosis, reversal is very difficult, resulting in a poor prognosis. There are many causes of liver fibrosis, including liver injury caused by drugs, viral hepatitis, alcoholic liver, fatty liver and autoimmune disease. The mechanism underlying hepatic fibrosis differs among etiologies. The establishment of an appropriate animal model of liver fibrosis is not only an important basis for the in-depth study of the pathogenesis of liver fibrosis but also an important means for clinical experts to select drugs for the prevention and treatment of liver fibrosis. The present study focused on the modeling methods and fibrosis characteristics of different animal models of liver fibrosis, such as a chemical-induced liver fibrosis model, autoimmune liver fibrosis model, cholestatic liver fibrosis model, alcoholic liver fibrosis model and non-alcoholic liver fibrosis model. In addition, we also summarize the research and application prospects concerning new organoids in liver fibrosis models proposed in recent years. A suitable animal model of liver fibrosis and organoid fibrosis model that closely resemble the physiological state of the human body will provide bases for the in-depth study of the pathogenesis of liver fibrosis and the development of therapeutic drugs. |
format | Online Article Text |
id | pubmed-8187919 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-81879192021-06-10 Animal and Organoid Models of Liver Fibrosis Bao, Yu-long Wang, Li Pan, Hai-ting Zhang, Tai-ran Chen, Ya-hong Xu, Shan-jing Mao, Xin-li Li, Shao-wei Front Physiol Physiology Liver fibrosis refers to the process underlying the development of chronic liver diseases, wherein liver cells are repeatedly destroyed and regenerated, which leads to an excessive deposition and abnormal distribution of the extracellular matrix such as collagen, glycoprotein and proteoglycan in the liver. Liver fibrosis thus constitutes the pathological repair response of the liver to chronic injury. Hepatic fibrosis is a key step in the progression of chronic liver disease to cirrhosis and an important factor affecting the prognosis of chronic liver disease. Further development of liver fibrosis may lead to structural disorders of the liver, nodular regeneration of hepatocytes and the formation of cirrhosis. Hepatic fibrosis is histologically reversible if treated aggressively during this period, but when fibrosis progresses to the stage of cirrhosis, reversal is very difficult, resulting in a poor prognosis. There are many causes of liver fibrosis, including liver injury caused by drugs, viral hepatitis, alcoholic liver, fatty liver and autoimmune disease. The mechanism underlying hepatic fibrosis differs among etiologies. The establishment of an appropriate animal model of liver fibrosis is not only an important basis for the in-depth study of the pathogenesis of liver fibrosis but also an important means for clinical experts to select drugs for the prevention and treatment of liver fibrosis. The present study focused on the modeling methods and fibrosis characteristics of different animal models of liver fibrosis, such as a chemical-induced liver fibrosis model, autoimmune liver fibrosis model, cholestatic liver fibrosis model, alcoholic liver fibrosis model and non-alcoholic liver fibrosis model. In addition, we also summarize the research and application prospects concerning new organoids in liver fibrosis models proposed in recent years. A suitable animal model of liver fibrosis and organoid fibrosis model that closely resemble the physiological state of the human body will provide bases for the in-depth study of the pathogenesis of liver fibrosis and the development of therapeutic drugs. Frontiers Media S.A. 2021-05-26 /pmc/articles/PMC8187919/ /pubmed/34122138 http://dx.doi.org/10.3389/fphys.2021.666138 Text en Copyright © 2021 Bao, Wang, Pan, Zhang, Chen, Xu, Mao and Li. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Physiology Bao, Yu-long Wang, Li Pan, Hai-ting Zhang, Tai-ran Chen, Ya-hong Xu, Shan-jing Mao, Xin-li Li, Shao-wei Animal and Organoid Models of Liver Fibrosis |
title | Animal and Organoid Models of Liver Fibrosis |
title_full | Animal and Organoid Models of Liver Fibrosis |
title_fullStr | Animal and Organoid Models of Liver Fibrosis |
title_full_unstemmed | Animal and Organoid Models of Liver Fibrosis |
title_short | Animal and Organoid Models of Liver Fibrosis |
title_sort | animal and organoid models of liver fibrosis |
topic | Physiology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8187919/ https://www.ncbi.nlm.nih.gov/pubmed/34122138 http://dx.doi.org/10.3389/fphys.2021.666138 |
work_keys_str_mv | AT baoyulong animalandorganoidmodelsofliverfibrosis AT wangli animalandorganoidmodelsofliverfibrosis AT panhaiting animalandorganoidmodelsofliverfibrosis AT zhangtairan animalandorganoidmodelsofliverfibrosis AT chenyahong animalandorganoidmodelsofliverfibrosis AT xushanjing animalandorganoidmodelsofliverfibrosis AT maoxinli animalandorganoidmodelsofliverfibrosis AT lishaowei animalandorganoidmodelsofliverfibrosis |