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Progress in the mechanism and targeted drug therapy for COPD
Chronic obstructive pulmonary disease (COPD) is emphysema and/or chronic bronchitis characterised by long-term breathing problems and poor airflow. The prevalence of COPD has increased over the last decade and the drugs most commonly used to treat it, such as glucocorticoids and bronchodilators, hav...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group UK
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7588592/ https://www.ncbi.nlm.nih.gov/pubmed/33110061 http://dx.doi.org/10.1038/s41392-020-00345-x |
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author | Wang, Cuixue Zhou, Jiedong Wang, Jinquan Li, Shujing Fukunaga, Atsushi Yodoi, Junji Tian, Hai |
author_facet | Wang, Cuixue Zhou, Jiedong Wang, Jinquan Li, Shujing Fukunaga, Atsushi Yodoi, Junji Tian, Hai |
author_sort | Wang, Cuixue |
collection | PubMed |
description | Chronic obstructive pulmonary disease (COPD) is emphysema and/or chronic bronchitis characterised by long-term breathing problems and poor airflow. The prevalence of COPD has increased over the last decade and the drugs most commonly used to treat it, such as glucocorticoids and bronchodilators, have significant therapeutic effects; however, they also cause side effects, including infection and immunosuppression. Here we reviewed the pathogenesis and progression of COPD and elaborated on the effects and mechanisms of newly developed molecular targeted COPD therapeutic drugs. Among these new drugs, we focussed on thioredoxin (Trx). Trx effectively prevents the progression of COPD by regulating redox status and protease/anti-protease balance, blocking the NF-κB and MAPK signalling pathways, suppressing the activation and migration of inflammatory cells and the production of cytokines, inhibiting the synthesis and the activation of adhesion factors and growth factors, and controlling the cAMP-PKA and PI3K/Akt signalling pathways. The mechanism by which Trx affects COPD is different from glucocorticoid-based mechanisms which regulate the inflammatory reaction in association with suppressing immune responses. In addition, Trx also improves the insensitivity of COPD to steroids by inhibiting the production and internalisation of macrophage migration inhibitory factor (MIF). Taken together, these findings suggest that Trx may be the ideal drug for treating COPD. |
format | Online Article Text |
id | pubmed-7588592 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-75885922020-10-27 Progress in the mechanism and targeted drug therapy for COPD Wang, Cuixue Zhou, Jiedong Wang, Jinquan Li, Shujing Fukunaga, Atsushi Yodoi, Junji Tian, Hai Signal Transduct Target Ther Review Article Chronic obstructive pulmonary disease (COPD) is emphysema and/or chronic bronchitis characterised by long-term breathing problems and poor airflow. The prevalence of COPD has increased over the last decade and the drugs most commonly used to treat it, such as glucocorticoids and bronchodilators, have significant therapeutic effects; however, they also cause side effects, including infection and immunosuppression. Here we reviewed the pathogenesis and progression of COPD and elaborated on the effects and mechanisms of newly developed molecular targeted COPD therapeutic drugs. Among these new drugs, we focussed on thioredoxin (Trx). Trx effectively prevents the progression of COPD by regulating redox status and protease/anti-protease balance, blocking the NF-κB and MAPK signalling pathways, suppressing the activation and migration of inflammatory cells and the production of cytokines, inhibiting the synthesis and the activation of adhesion factors and growth factors, and controlling the cAMP-PKA and PI3K/Akt signalling pathways. The mechanism by which Trx affects COPD is different from glucocorticoid-based mechanisms which regulate the inflammatory reaction in association with suppressing immune responses. In addition, Trx also improves the insensitivity of COPD to steroids by inhibiting the production and internalisation of macrophage migration inhibitory factor (MIF). Taken together, these findings suggest that Trx may be the ideal drug for treating COPD. Nature Publishing Group UK 2020-10-27 /pmc/articles/PMC7588592/ /pubmed/33110061 http://dx.doi.org/10.1038/s41392-020-00345-x Text en © The Author(s) 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Review Article Wang, Cuixue Zhou, Jiedong Wang, Jinquan Li, Shujing Fukunaga, Atsushi Yodoi, Junji Tian, Hai Progress in the mechanism and targeted drug therapy for COPD |
title | Progress in the mechanism and targeted drug therapy for COPD |
title_full | Progress in the mechanism and targeted drug therapy for COPD |
title_fullStr | Progress in the mechanism and targeted drug therapy for COPD |
title_full_unstemmed | Progress in the mechanism and targeted drug therapy for COPD |
title_short | Progress in the mechanism and targeted drug therapy for COPD |
title_sort | progress in the mechanism and targeted drug therapy for copd |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7588592/ https://www.ncbi.nlm.nih.gov/pubmed/33110061 http://dx.doi.org/10.1038/s41392-020-00345-x |
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