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Liver Fibrosis Resolution: From Molecular Mechanisms to Therapeutic Opportunities

The liver is a critical system for metabolism in human beings, which plays an essential role in an abundance of physiological processes and is vulnerable to endogenous or exogenous injuries. After the damage to the liver, a type of aberrant wound healing response known as liver fibrosis may happen,...

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Autores principales: Pei, Qiying, Yi, Qian, Tang, Liling
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10253436/
https://www.ncbi.nlm.nih.gov/pubmed/37298621
http://dx.doi.org/10.3390/ijms24119671
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author Pei, Qiying
Yi, Qian
Tang, Liling
author_facet Pei, Qiying
Yi, Qian
Tang, Liling
author_sort Pei, Qiying
collection PubMed
description The liver is a critical system for metabolism in human beings, which plays an essential role in an abundance of physiological processes and is vulnerable to endogenous or exogenous injuries. After the damage to the liver, a type of aberrant wound healing response known as liver fibrosis may happen, which can result in an excessive accumulation of extracellular matrix (ECM) and then cause cirrhosis or hepatocellular carcinoma (HCC), seriously endangering human health and causing a great economic burden. However, few effective anti-fibrotic medications are clinically available to treat liver fibrosis. The most efficient approach to liver fibrosis prevention and treatment currently is to eliminate its causes, but this approach’s efficiency is too slow, or some causes cannot be fully eliminated, which causes liver fibrosis to worsen. In cases of advanced fibrosis, the only available treatment is liver transplantation. Therefore, new treatments or therapeutic agents need to be explored to stop the further development of early liver fibrosis or to reverse the fibrosis process to achieve liver fibrosis resolution. Understanding the mechanisms that lead to the development of liver fibrosis is necessary to find new therapeutic targets and drugs. The complex process of liver fibrosis is regulated by a variety of cells and cytokines, among which hepatic stellate cells (HSCs) are the essential cells, and their continued activation will lead to further progression of liver fibrosis. It has been found that inhibiting HSC activation, or inducing apoptosis, and inactivating activated hepatic stellate cells (aHSCs) can reverse fibrosis and thus achieve liver fibrosis regression. Hence, this review will concentrate on how HSCs become activated during liver fibrosis, including intercellular interactions and related signaling pathways, as well as targeting HSCs or liver fibrosis signaling pathways to achieve the resolution of liver fibrosis. Finally, new therapeutic compounds targeting liver fibrosis are summarized to provide more options for the therapy of liver fibrosis.
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spelling pubmed-102534362023-06-10 Liver Fibrosis Resolution: From Molecular Mechanisms to Therapeutic Opportunities Pei, Qiying Yi, Qian Tang, Liling Int J Mol Sci Review The liver is a critical system for metabolism in human beings, which plays an essential role in an abundance of physiological processes and is vulnerable to endogenous or exogenous injuries. After the damage to the liver, a type of aberrant wound healing response known as liver fibrosis may happen, which can result in an excessive accumulation of extracellular matrix (ECM) and then cause cirrhosis or hepatocellular carcinoma (HCC), seriously endangering human health and causing a great economic burden. However, few effective anti-fibrotic medications are clinically available to treat liver fibrosis. The most efficient approach to liver fibrosis prevention and treatment currently is to eliminate its causes, but this approach’s efficiency is too slow, or some causes cannot be fully eliminated, which causes liver fibrosis to worsen. In cases of advanced fibrosis, the only available treatment is liver transplantation. Therefore, new treatments or therapeutic agents need to be explored to stop the further development of early liver fibrosis or to reverse the fibrosis process to achieve liver fibrosis resolution. Understanding the mechanisms that lead to the development of liver fibrosis is necessary to find new therapeutic targets and drugs. The complex process of liver fibrosis is regulated by a variety of cells and cytokines, among which hepatic stellate cells (HSCs) are the essential cells, and their continued activation will lead to further progression of liver fibrosis. It has been found that inhibiting HSC activation, or inducing apoptosis, and inactivating activated hepatic stellate cells (aHSCs) can reverse fibrosis and thus achieve liver fibrosis regression. Hence, this review will concentrate on how HSCs become activated during liver fibrosis, including intercellular interactions and related signaling pathways, as well as targeting HSCs or liver fibrosis signaling pathways to achieve the resolution of liver fibrosis. Finally, new therapeutic compounds targeting liver fibrosis are summarized to provide more options for the therapy of liver fibrosis. MDPI 2023-06-02 /pmc/articles/PMC10253436/ /pubmed/37298621 http://dx.doi.org/10.3390/ijms24119671 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Pei, Qiying
Yi, Qian
Tang, Liling
Liver Fibrosis Resolution: From Molecular Mechanisms to Therapeutic Opportunities
title Liver Fibrosis Resolution: From Molecular Mechanisms to Therapeutic Opportunities
title_full Liver Fibrosis Resolution: From Molecular Mechanisms to Therapeutic Opportunities
title_fullStr Liver Fibrosis Resolution: From Molecular Mechanisms to Therapeutic Opportunities
title_full_unstemmed Liver Fibrosis Resolution: From Molecular Mechanisms to Therapeutic Opportunities
title_short Liver Fibrosis Resolution: From Molecular Mechanisms to Therapeutic Opportunities
title_sort liver fibrosis resolution: from molecular mechanisms to therapeutic opportunities
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10253436/
https://www.ncbi.nlm.nih.gov/pubmed/37298621
http://dx.doi.org/10.3390/ijms24119671
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AT yiqian liverfibrosisresolutionfrommolecularmechanismstotherapeuticopportunities
AT tangliling liverfibrosisresolutionfrommolecularmechanismstotherapeuticopportunities