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Ubiquitination in Scleroderma Fibrosis and Its Treatment
Scleroderma (systemic sclerosis, SSc) is a highly heterogeneous rheumatic disease, and uncontrolled fibrosis in visceral organs is the major cause of death in patients. The transforming growth factor-β (TGF-β) and WNT/β-catenin signaling pathways, along with signal transducer and activator of transc...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6199354/ https://www.ncbi.nlm.nih.gov/pubmed/30386338 http://dx.doi.org/10.3389/fimmu.2018.02383 |
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author | Long, Ying Chen, Weilin Du, Qian Zuo, Xiaoxia Zhu, Honglin |
author_facet | Long, Ying Chen, Weilin Du, Qian Zuo, Xiaoxia Zhu, Honglin |
author_sort | Long, Ying |
collection | PubMed |
description | Scleroderma (systemic sclerosis, SSc) is a highly heterogeneous rheumatic disease, and uncontrolled fibrosis in visceral organs is the major cause of death in patients. The transforming growth factor-β (TGF-β) and WNT/β-catenin signaling pathways, along with signal transducer and activator of transcription 3 (STAT3), play crucial roles in this fibrotic process. Currently, no therapy is available that effectively arrests or reverses the progression of fibrosis in patients with SSc. Ubiquitination is an important post-translational modification that controls many critical cellular functions. Dysregulated ubiquitination events have been observed in patients with systemic lupus erythematosus, rheumatoid arthritis and fibrotic diseases. Inhibitors targeting the ubiquitination pathway have considerable potential for the treatment of rheumatic diseases. However, very few studies have examined the role and mechanism of ubiquitination in patients with SSc. In this review, we will summarize the molecular mechanisms of ubiquitination in patients with SSc and explore the potential targets for treatment. |
format | Online Article Text |
id | pubmed-6199354 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-61993542018-11-01 Ubiquitination in Scleroderma Fibrosis and Its Treatment Long, Ying Chen, Weilin Du, Qian Zuo, Xiaoxia Zhu, Honglin Front Immunol Immunology Scleroderma (systemic sclerosis, SSc) is a highly heterogeneous rheumatic disease, and uncontrolled fibrosis in visceral organs is the major cause of death in patients. The transforming growth factor-β (TGF-β) and WNT/β-catenin signaling pathways, along with signal transducer and activator of transcription 3 (STAT3), play crucial roles in this fibrotic process. Currently, no therapy is available that effectively arrests or reverses the progression of fibrosis in patients with SSc. Ubiquitination is an important post-translational modification that controls many critical cellular functions. Dysregulated ubiquitination events have been observed in patients with systemic lupus erythematosus, rheumatoid arthritis and fibrotic diseases. Inhibitors targeting the ubiquitination pathway have considerable potential for the treatment of rheumatic diseases. However, very few studies have examined the role and mechanism of ubiquitination in patients with SSc. In this review, we will summarize the molecular mechanisms of ubiquitination in patients with SSc and explore the potential targets for treatment. Frontiers Media S.A. 2018-10-17 /pmc/articles/PMC6199354/ /pubmed/30386338 http://dx.doi.org/10.3389/fimmu.2018.02383 Text en Copyright © 2018 Long, Chen, Du, Zuo and Zhu. http://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 Long, Ying Chen, Weilin Du, Qian Zuo, Xiaoxia Zhu, Honglin Ubiquitination in Scleroderma Fibrosis and Its Treatment |
title | Ubiquitination in Scleroderma Fibrosis and Its Treatment |
title_full | Ubiquitination in Scleroderma Fibrosis and Its Treatment |
title_fullStr | Ubiquitination in Scleroderma Fibrosis and Its Treatment |
title_full_unstemmed | Ubiquitination in Scleroderma Fibrosis and Its Treatment |
title_short | Ubiquitination in Scleroderma Fibrosis and Its Treatment |
title_sort | ubiquitination in scleroderma fibrosis and its treatment |
topic | Immunology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6199354/ https://www.ncbi.nlm.nih.gov/pubmed/30386338 http://dx.doi.org/10.3389/fimmu.2018.02383 |
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