Pathological Insight into 5-HT<sub>2B</sub> Receptor Activation in Fibrosing Interstitial Lung Diseases
Interstitial lung disease (ILD) encompasses a heterogeneous group of more than 200 conditions, of which primarily idiopathic pulmonary fibrosis (IPF), idiopathic nonspecific interstitial pneumonia, hypersensitivity pneumonitis, ILD associated with autoimmune diseases and sarcoidosis may present a pr...
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MDPI AG
2020-12-01
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Online Access: | https://www.mdpi.com/1422-0067/22/1/225 |
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author | Anna Löfdahl Göran Tornling Jenny Wigén Anna-Karin Larsson-Callerfelt Christina Wenglén Gunilla Westergren-Thorsson |
author_facet | Anna Löfdahl Göran Tornling Jenny Wigén Anna-Karin Larsson-Callerfelt Christina Wenglén Gunilla Westergren-Thorsson |
author_sort | Anna Löfdahl |
collection | DOAJ |
description | Interstitial lung disease (ILD) encompasses a heterogeneous group of more than 200 conditions, of which primarily idiopathic pulmonary fibrosis (IPF), idiopathic nonspecific interstitial pneumonia, hypersensitivity pneumonitis, ILD associated with autoimmune diseases and sarcoidosis may present a progressive fibrosing (PF) phenotype. Despite different aetiology and histopathological patterns, the PF-ILDs have similarities regarding disease mechanisms with self-sustaining fibrosis, which suggests that the diseases may share common pathogenetic pathways. Previous studies show an enhanced activation of serotonergic signaling in pulmonary fibrosis, and the serotonin (5-HT)<sub>2</sub> receptors have been implicated to have important roles in observed profibrotic actions. Our research findings in support by others, demonstrate antifibrotic effects with 5-HT<sub>2B</sub> receptor antagonists, alleviating several key events common for the fibrotic diseases such as myofibroblast differentiation and connective tissue deposition. In this review, we will address the potential role of 5-HT and in particular the 5-HT<sub>2B</sub> receptors in three PF-ILDs: ILD associated with systemic sclerosis (SSc-ILD), ILD associated with rheumatoid arthritis (RA-ILD) and IPF. Highlighting the converging pathways in these diseases discloses the 5-HT<sub>2B</sub> receptor as a potential disease target for PF-ILDs, which today have an urgent unmet need for therapeutic strategies. |
first_indexed | 2024-03-10T13:42:48Z |
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issn | 1661-6596 1422-0067 |
language | English |
last_indexed | 2024-03-10T13:42:48Z |
publishDate | 2020-12-01 |
publisher | MDPI AG |
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series | International Journal of Molecular Sciences |
spelling | doaj.art-925f74e01239493094019816af71eb2e2023-11-21T02:51:30ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672020-12-0122122510.3390/ijms22010225Pathological Insight into 5-HT<sub>2B</sub> Receptor Activation in Fibrosing Interstitial Lung DiseasesAnna Löfdahl0Göran Tornling1Jenny Wigén2Anna-Karin Larsson-Callerfelt3Christina Wenglén4Gunilla Westergren-Thorsson5Lung Biology, Department of Experimental Medical Science, Lund University, BMC C12, 22184 Lund, SwedenAnaMar AB, Medicon Village, Scheeletorget 1, 22381 Lund, SwedenLung Biology, Department of Experimental Medical Science, Lund University, BMC C12, 22184 Lund, SwedenLung Biology, Department of Experimental Medical Science, Lund University, BMC C12, 22184 Lund, SwedenAnaMar AB, Medicon Village, Scheeletorget 1, 22381 Lund, SwedenLung Biology, Department of Experimental Medical Science, Lund University, BMC C12, 22184 Lund, SwedenInterstitial lung disease (ILD) encompasses a heterogeneous group of more than 200 conditions, of which primarily idiopathic pulmonary fibrosis (IPF), idiopathic nonspecific interstitial pneumonia, hypersensitivity pneumonitis, ILD associated with autoimmune diseases and sarcoidosis may present a progressive fibrosing (PF) phenotype. Despite different aetiology and histopathological patterns, the PF-ILDs have similarities regarding disease mechanisms with self-sustaining fibrosis, which suggests that the diseases may share common pathogenetic pathways. Previous studies show an enhanced activation of serotonergic signaling in pulmonary fibrosis, and the serotonin (5-HT)<sub>2</sub> receptors have been implicated to have important roles in observed profibrotic actions. Our research findings in support by others, demonstrate antifibrotic effects with 5-HT<sub>2B</sub> receptor antagonists, alleviating several key events common for the fibrotic diseases such as myofibroblast differentiation and connective tissue deposition. In this review, we will address the potential role of 5-HT and in particular the 5-HT<sub>2B</sub> receptors in three PF-ILDs: ILD associated with systemic sclerosis (SSc-ILD), ILD associated with rheumatoid arthritis (RA-ILD) and IPF. Highlighting the converging pathways in these diseases discloses the 5-HT<sub>2B</sub> receptor as a potential disease target for PF-ILDs, which today have an urgent unmet need for therapeutic strategies.https://www.mdpi.com/1422-0067/22/1/2255-HT5-HT<sub>2B</sub> receptor antagonismfibrosisILD |
spellingShingle | Anna Löfdahl Göran Tornling Jenny Wigén Anna-Karin Larsson-Callerfelt Christina Wenglén Gunilla Westergren-Thorsson Pathological Insight into 5-HT<sub>2B</sub> Receptor Activation in Fibrosing Interstitial Lung Diseases International Journal of Molecular Sciences 5-HT 5-HT<sub>2B</sub> receptor antagonism fibrosis ILD |
title | Pathological Insight into 5-HT<sub>2B</sub> Receptor Activation in Fibrosing Interstitial Lung Diseases |
title_full | Pathological Insight into 5-HT<sub>2B</sub> Receptor Activation in Fibrosing Interstitial Lung Diseases |
title_fullStr | Pathological Insight into 5-HT<sub>2B</sub> Receptor Activation in Fibrosing Interstitial Lung Diseases |
title_full_unstemmed | Pathological Insight into 5-HT<sub>2B</sub> Receptor Activation in Fibrosing Interstitial Lung Diseases |
title_short | Pathological Insight into 5-HT<sub>2B</sub> Receptor Activation in Fibrosing Interstitial Lung Diseases |
title_sort | pathological insight into 5 ht sub 2b sub receptor activation in fibrosing interstitial lung diseases |
topic | 5-HT 5-HT<sub>2B</sub> receptor antagonism fibrosis ILD |
url | https://www.mdpi.com/1422-0067/22/1/225 |
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