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The role of Mesothelin signaling in Portal Fibroblasts in the pathogenesis of cholestatic liver fibrosis
Liver fibrosis develops in response to chronic toxic or cholestatic injury, and is characterized by apoptosis of damaged hepatocytes, development of inflammatory responses, and activation of Collagen Type I producing myofibroblasts that make liver fibrotic. Two major cell types, Hepatic Stellate Cel...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8710774/ https://www.ncbi.nlm.nih.gov/pubmed/34966784 http://dx.doi.org/10.3389/fmolb.2021.790032 |
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author | Fuji, Hiroaki Miller, Grant Nishio, Takahiro Koyama, Yukinori Lam, Kevin Zhang, Vivian Loomba, Rohit Brenner, David Kisseleva, Tatiana |
author_facet | Fuji, Hiroaki Miller, Grant Nishio, Takahiro Koyama, Yukinori Lam, Kevin Zhang, Vivian Loomba, Rohit Brenner, David Kisseleva, Tatiana |
author_sort | Fuji, Hiroaki |
collection | PubMed |
description | Liver fibrosis develops in response to chronic toxic or cholestatic injury, and is characterized by apoptosis of damaged hepatocytes, development of inflammatory responses, and activation of Collagen Type I producing myofibroblasts that make liver fibrotic. Two major cell types, Hepatic Stellate Cells (HSCs) and Portal Fibroblasts (PFs) are the major source of hepatic myofibroblasts. Hepatotoxic liver injury activates Hepatic Stellate Cells (aHSCs) to become myofibroblasts, while cholestatic liver injury activates both aHSCs and Portal Fibroblasts (aPFs). aPFs comprise the major population of myofibroblasts at the onset of cholestatic injury, while aHSCs are increasingly activated with fibrosis progression. Here we summarize our current understanding of the role of aPFs in the pathogenesis of cholestatic fibrosis, their unique features, and outline the potential mechanism of targeting aPFs in fibrotic liver. |
format | Online Article Text |
id | pubmed-8710774 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-87107742021-12-28 The role of Mesothelin signaling in Portal Fibroblasts in the pathogenesis of cholestatic liver fibrosis Fuji, Hiroaki Miller, Grant Nishio, Takahiro Koyama, Yukinori Lam, Kevin Zhang, Vivian Loomba, Rohit Brenner, David Kisseleva, Tatiana Front Mol Biosci Molecular Biosciences Liver fibrosis develops in response to chronic toxic or cholestatic injury, and is characterized by apoptosis of damaged hepatocytes, development of inflammatory responses, and activation of Collagen Type I producing myofibroblasts that make liver fibrotic. Two major cell types, Hepatic Stellate Cells (HSCs) and Portal Fibroblasts (PFs) are the major source of hepatic myofibroblasts. Hepatotoxic liver injury activates Hepatic Stellate Cells (aHSCs) to become myofibroblasts, while cholestatic liver injury activates both aHSCs and Portal Fibroblasts (aPFs). aPFs comprise the major population of myofibroblasts at the onset of cholestatic injury, while aHSCs are increasingly activated with fibrosis progression. Here we summarize our current understanding of the role of aPFs in the pathogenesis of cholestatic fibrosis, their unique features, and outline the potential mechanism of targeting aPFs in fibrotic liver. Frontiers Media S.A. 2021-12-13 /pmc/articles/PMC8710774/ /pubmed/34966784 http://dx.doi.org/10.3389/fmolb.2021.790032 Text en Copyright © 2021 Fuji, Miller, Nishio, Koyama, Lam, Zhang, Loomba, Brenner and Kisseleva. 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 | Molecular Biosciences Fuji, Hiroaki Miller, Grant Nishio, Takahiro Koyama, Yukinori Lam, Kevin Zhang, Vivian Loomba, Rohit Brenner, David Kisseleva, Tatiana The role of Mesothelin signaling in Portal Fibroblasts in the pathogenesis of cholestatic liver fibrosis |
title | The role of Mesothelin signaling in Portal Fibroblasts in the pathogenesis of cholestatic liver fibrosis |
title_full | The role of Mesothelin signaling in Portal Fibroblasts in the pathogenesis of cholestatic liver fibrosis |
title_fullStr | The role of Mesothelin signaling in Portal Fibroblasts in the pathogenesis of cholestatic liver fibrosis |
title_full_unstemmed | The role of Mesothelin signaling in Portal Fibroblasts in the pathogenesis of cholestatic liver fibrosis |
title_short | The role of Mesothelin signaling in Portal Fibroblasts in the pathogenesis of cholestatic liver fibrosis |
title_sort | role of mesothelin signaling in portal fibroblasts in the pathogenesis of cholestatic liver fibrosis |
topic | Molecular Biosciences |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8710774/ https://www.ncbi.nlm.nih.gov/pubmed/34966784 http://dx.doi.org/10.3389/fmolb.2021.790032 |
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