Approach for Elucidating the Molecular Mechanism of Epithelial to Mesenchymal Transition in Fibrosis of Asthmatic Airway Remodeling Focusing on Cl<sup>−</sup> Channels
Airway remodeling caused by asthma is characterized by structural changes of subepithelial fibrosis, goblet cell metaplasia, submucosal gland hyperplasia, smooth muscle cell hyperplasia, and angiogenesis, leading to symptoms such as dyspnea, which cause marked quality of life deterioration. In parti...
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| Format: | Article |
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MDPI AG
2023-12-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/25/1/289 |
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| author | Susumu Yoshie Shigeyuki Murono Akihiro Hazama |
| author_facet | Susumu Yoshie Shigeyuki Murono Akihiro Hazama |
| author_sort | Susumu Yoshie |
| collection | DOAJ |
| description | Airway remodeling caused by asthma is characterized by structural changes of subepithelial fibrosis, goblet cell metaplasia, submucosal gland hyperplasia, smooth muscle cell hyperplasia, and angiogenesis, leading to symptoms such as dyspnea, which cause marked quality of life deterioration. In particular, fibrosis exacerbated by asthma progression is reportedly mediated by epithelial-mesenchymal transition (EMT). It is well known that the molecular mechanism of EMT in fibrosis of asthmatic airway remodeling is closely associated with several signaling pathways, including the TGF-β1/Smad, TGF-β1/non-Smad, and Wnt/β-catenin signaling pathways. However, the molecular mechanism of EMT in fibrosis of asthmatic airway remodeling has not yet been fully clarified. Given that Cl<sup>−</sup> transport through Cl<sup>−</sup> channels causes passive water flow and consequent changes in cell volume, these channels may be considered to play a key role in EMT, which is characterized by significant morphological changes. In the present article, we highlight how EMT, which causes fibrosis and carcinogenesis in various tissues, is strongly associated with activation or inactivation of Cl<sup>−</sup> channels and discuss whether Cl<sup>−</sup> channels can lead to elucidation of the molecular mechanism of EMT in fibrosis of asthmatic airway remodeling. |
| first_indexed | 2024-03-08T15:05:29Z |
| format | Article |
| id | doaj.art-8dc68756713b4635b45cb82fb9588600 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-08T15:05:29Z |
| publishDate | 2023-12-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-8dc68756713b4635b45cb82fb95886002024-01-10T14:58:53ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672023-12-0125128910.3390/ijms25010289Approach for Elucidating the Molecular Mechanism of Epithelial to Mesenchymal Transition in Fibrosis of Asthmatic Airway Remodeling Focusing on Cl<sup>−</sup> ChannelsSusumu Yoshie0Shigeyuki Murono1Akihiro Hazama2Department of Cellular and Integrative Physiology, Graduate School of Medicine, Fukushima Medical University, Fukushima 960-1295, JapanDepartment of Otolaryngology Head and Neck Surgery, Graduate School of Medicine, Fukushima Medical University, Fukushima 960-1295, JapanDepartment of Cellular and Integrative Physiology, Graduate School of Medicine, Fukushima Medical University, Fukushima 960-1295, JapanAirway remodeling caused by asthma is characterized by structural changes of subepithelial fibrosis, goblet cell metaplasia, submucosal gland hyperplasia, smooth muscle cell hyperplasia, and angiogenesis, leading to symptoms such as dyspnea, which cause marked quality of life deterioration. In particular, fibrosis exacerbated by asthma progression is reportedly mediated by epithelial-mesenchymal transition (EMT). It is well known that the molecular mechanism of EMT in fibrosis of asthmatic airway remodeling is closely associated with several signaling pathways, including the TGF-β1/Smad, TGF-β1/non-Smad, and Wnt/β-catenin signaling pathways. However, the molecular mechanism of EMT in fibrosis of asthmatic airway remodeling has not yet been fully clarified. Given that Cl<sup>−</sup> transport through Cl<sup>−</sup> channels causes passive water flow and consequent changes in cell volume, these channels may be considered to play a key role in EMT, which is characterized by significant morphological changes. In the present article, we highlight how EMT, which causes fibrosis and carcinogenesis in various tissues, is strongly associated with activation or inactivation of Cl<sup>−</sup> channels and discuss whether Cl<sup>−</sup> channels can lead to elucidation of the molecular mechanism of EMT in fibrosis of asthmatic airway remodeling.https://www.mdpi.com/1422-0067/25/1/289asthmaairwayfibrosisepithelial to mesenchymal transitionCl<sup>−</sup> channelcell volume |
| spellingShingle | Susumu Yoshie Shigeyuki Murono Akihiro Hazama Approach for Elucidating the Molecular Mechanism of Epithelial to Mesenchymal Transition in Fibrosis of Asthmatic Airway Remodeling Focusing on Cl<sup>−</sup> Channels International Journal of Molecular Sciences asthma airway fibrosis epithelial to mesenchymal transition Cl<sup>−</sup> channel cell volume |
| title | Approach for Elucidating the Molecular Mechanism of Epithelial to Mesenchymal Transition in Fibrosis of Asthmatic Airway Remodeling Focusing on Cl<sup>−</sup> Channels |
| title_full | Approach for Elucidating the Molecular Mechanism of Epithelial to Mesenchymal Transition in Fibrosis of Asthmatic Airway Remodeling Focusing on Cl<sup>−</sup> Channels |
| title_fullStr | Approach for Elucidating the Molecular Mechanism of Epithelial to Mesenchymal Transition in Fibrosis of Asthmatic Airway Remodeling Focusing on Cl<sup>−</sup> Channels |
| title_full_unstemmed | Approach for Elucidating the Molecular Mechanism of Epithelial to Mesenchymal Transition in Fibrosis of Asthmatic Airway Remodeling Focusing on Cl<sup>−</sup> Channels |
| title_short | Approach for Elucidating the Molecular Mechanism of Epithelial to Mesenchymal Transition in Fibrosis of Asthmatic Airway Remodeling Focusing on Cl<sup>−</sup> Channels |
| title_sort | approach for elucidating the molecular mechanism of epithelial to mesenchymal transition in fibrosis of asthmatic airway remodeling focusing on cl sup sup channels |
| topic | asthma airway fibrosis epithelial to mesenchymal transition Cl<sup>−</sup> channel cell volume |
| url | https://www.mdpi.com/1422-0067/25/1/289 |
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