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The role of the macrophage-to-myofibroblast transition in renal fibrosis

Renal fibrosis causes structural and functional impairment of the kidney, which is a dominant component of chronic kidney disease. Recently, a novel mechanism, macrophage-to-myofibroblast transition (MMT), has been identified as a crucial component in renal fibrosis as a response to chronic inflamma...

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Detalles Bibliográficos
Autores principales: Wei, Jia, Xu, Zihao, Yan, Xiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9389037/
https://www.ncbi.nlm.nih.gov/pubmed/35990655
http://dx.doi.org/10.3389/fimmu.2022.934377
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author Wei, Jia
Xu, Zihao
Yan, Xiang
author_facet Wei, Jia
Xu, Zihao
Yan, Xiang
author_sort Wei, Jia
collection PubMed
description Renal fibrosis causes structural and functional impairment of the kidney, which is a dominant component of chronic kidney disease. Recently, a novel mechanism, macrophage-to-myofibroblast transition (MMT), has been identified as a crucial component in renal fibrosis as a response to chronic inflammation. It is a process by which bone marrow-derived macrophages differentiate into myofibroblasts during renal injury and promote renal fibrosis. Here, we summarized recent evidence and mechanisms of MMT in renal fibrosis. Understanding this phenomenon and its underlying signal pathway would be beneficial to find therapeutic targets for renal fibrosis in chronic kidney disease.
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spelling pubmed-93890372022-08-20 The role of the macrophage-to-myofibroblast transition in renal fibrosis Wei, Jia Xu, Zihao Yan, Xiang Front Immunol Immunology Renal fibrosis causes structural and functional impairment of the kidney, which is a dominant component of chronic kidney disease. Recently, a novel mechanism, macrophage-to-myofibroblast transition (MMT), has been identified as a crucial component in renal fibrosis as a response to chronic inflammation. It is a process by which bone marrow-derived macrophages differentiate into myofibroblasts during renal injury and promote renal fibrosis. Here, we summarized recent evidence and mechanisms of MMT in renal fibrosis. Understanding this phenomenon and its underlying signal pathway would be beneficial to find therapeutic targets for renal fibrosis in chronic kidney disease. Frontiers Media S.A. 2022-08-05 /pmc/articles/PMC9389037/ /pubmed/35990655 http://dx.doi.org/10.3389/fimmu.2022.934377 Text en Copyright © 2022 Wei, Xu and Yan 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 Immunology
Wei, Jia
Xu, Zihao
Yan, Xiang
The role of the macrophage-to-myofibroblast transition in renal fibrosis
title The role of the macrophage-to-myofibroblast transition in renal fibrosis
title_full The role of the macrophage-to-myofibroblast transition in renal fibrosis
title_fullStr The role of the macrophage-to-myofibroblast transition in renal fibrosis
title_full_unstemmed The role of the macrophage-to-myofibroblast transition in renal fibrosis
title_short The role of the macrophage-to-myofibroblast transition in renal fibrosis
title_sort role of the macrophage-to-myofibroblast transition in renal fibrosis
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9389037/
https://www.ncbi.nlm.nih.gov/pubmed/35990655
http://dx.doi.org/10.3389/fimmu.2022.934377
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