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The Role of JAK/STAT Pathway in Fibrotic Diseases: Molecular and Cellular Mechanisms

There are four members of the JAK family and seven of the STAT family in mammals. The JAK/STAT molecular pathway could be activated by broad hormones, cytokines, growth factors, and more. The JAK/STAT signaling pathway extensively mediates various biological processes such as cell proliferation, dif...

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Detalles Bibliográficos
Autores principales: Liu, Jia, Wang, Faping, Luo, Fengming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9855819/
https://www.ncbi.nlm.nih.gov/pubmed/36671504
http://dx.doi.org/10.3390/biom13010119
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author Liu, Jia
Wang, Faping
Luo, Fengming
author_facet Liu, Jia
Wang, Faping
Luo, Fengming
author_sort Liu, Jia
collection PubMed
description There are four members of the JAK family and seven of the STAT family in mammals. The JAK/STAT molecular pathway could be activated by broad hormones, cytokines, growth factors, and more. The JAK/STAT signaling pathway extensively mediates various biological processes such as cell proliferation, differentiation, migration, apoptosis, and immune regulation. JAK/STAT activation is closely related to growth and development, homeostasis, various solid tumors, inflammatory illness, and autoimmune diseases. Recently, with the deepening understanding of the JAK/STAT pathway, the relationship between JAK/STAT and the pathophysiology of fibrotic diseases was noticed, including the liver, renal, heart, bone marrow, and lung. JAK inhibitor has been approved for myelofibrosis, and subsequently, JAK/STAT may serve as a promising target for fibrosis in other organs. Therefore, this article reviews the roles and mechanisms of the JAK/STAT signaling pathway in fibrotic diseases.
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spelling pubmed-98558192023-01-21 The Role of JAK/STAT Pathway in Fibrotic Diseases: Molecular and Cellular Mechanisms Liu, Jia Wang, Faping Luo, Fengming Biomolecules Review There are four members of the JAK family and seven of the STAT family in mammals. The JAK/STAT molecular pathway could be activated by broad hormones, cytokines, growth factors, and more. The JAK/STAT signaling pathway extensively mediates various biological processes such as cell proliferation, differentiation, migration, apoptosis, and immune regulation. JAK/STAT activation is closely related to growth and development, homeostasis, various solid tumors, inflammatory illness, and autoimmune diseases. Recently, with the deepening understanding of the JAK/STAT pathway, the relationship between JAK/STAT and the pathophysiology of fibrotic diseases was noticed, including the liver, renal, heart, bone marrow, and lung. JAK inhibitor has been approved for myelofibrosis, and subsequently, JAK/STAT may serve as a promising target for fibrosis in other organs. Therefore, this article reviews the roles and mechanisms of the JAK/STAT signaling pathway in fibrotic diseases. MDPI 2023-01-06 /pmc/articles/PMC9855819/ /pubmed/36671504 http://dx.doi.org/10.3390/biom13010119 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
Liu, Jia
Wang, Faping
Luo, Fengming
The Role of JAK/STAT Pathway in Fibrotic Diseases: Molecular and Cellular Mechanisms
title The Role of JAK/STAT Pathway in Fibrotic Diseases: Molecular and Cellular Mechanisms
title_full The Role of JAK/STAT Pathway in Fibrotic Diseases: Molecular and Cellular Mechanisms
title_fullStr The Role of JAK/STAT Pathway in Fibrotic Diseases: Molecular and Cellular Mechanisms
title_full_unstemmed The Role of JAK/STAT Pathway in Fibrotic Diseases: Molecular and Cellular Mechanisms
title_short The Role of JAK/STAT Pathway in Fibrotic Diseases: Molecular and Cellular Mechanisms
title_sort role of jak/stat pathway in fibrotic diseases: molecular and cellular mechanisms
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9855819/
https://www.ncbi.nlm.nih.gov/pubmed/36671504
http://dx.doi.org/10.3390/biom13010119
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