Small-molecule-mediated OGG1 inhibition attenuates pulmonary inflammation and lung fibrosis in a murine lung fibrosis model
Idiopathic pulmonary fibrosis is a disease caused by persistent micro-injuries to the lung ultimately resulting in death. Here, the authors describe the use of a small molecule OGG1 inhibitor, TH5487, as a potent and potentially clinically relevant treatment for IPF.
Main Authors: | , , , , , , , , , , , , , , , , , , |
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Format: | Article |
Language: | English |
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Nature Portfolio
2023-02-01
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Series: | Nature Communications |
Online Access: | https://doi.org/10.1038/s41467-023-36314-5 |
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author | L. Tanner A. B. Single R. K. V. Bhongir M. Heusel T. Mohanty C. A. Q. Karlsson L. Pan C-M. Clausson J. Bergwik K. Wang C. K. Andersson R. M. Oommen J. S. Erjefält J. Malmström O. Wallner I. Boldogh T. Helleday C. Kalderén A. Egesten |
author_facet | L. Tanner A. B. Single R. K. V. Bhongir M. Heusel T. Mohanty C. A. Q. Karlsson L. Pan C-M. Clausson J. Bergwik K. Wang C. K. Andersson R. M. Oommen J. S. Erjefält J. Malmström O. Wallner I. Boldogh T. Helleday C. Kalderén A. Egesten |
author_sort | L. Tanner |
collection | DOAJ |
description | Idiopathic pulmonary fibrosis is a disease caused by persistent micro-injuries to the lung ultimately resulting in death. Here, the authors describe the use of a small molecule OGG1 inhibitor, TH5487, as a potent and potentially clinically relevant treatment for IPF. |
first_indexed | 2024-04-10T15:42:54Z |
format | Article |
id | doaj.art-0623b68eecdd460eb6a8d722cb5c2edb |
institution | Directory Open Access Journal |
issn | 2041-1723 |
language | English |
last_indexed | 2024-04-10T15:42:54Z |
publishDate | 2023-02-01 |
publisher | Nature Portfolio |
record_format | Article |
series | Nature Communications |
spelling | doaj.art-0623b68eecdd460eb6a8d722cb5c2edb2023-02-12T12:17:18ZengNature PortfolioNature Communications2041-17232023-02-0114111610.1038/s41467-023-36314-5Small-molecule-mediated OGG1 inhibition attenuates pulmonary inflammation and lung fibrosis in a murine lung fibrosis modelL. Tanner0A. B. Single1R. K. V. Bhongir2M. Heusel3T. Mohanty4C. A. Q. Karlsson5L. Pan6C-M. Clausson7J. Bergwik8K. Wang9C. K. Andersson10R. M. Oommen11J. S. Erjefält12J. Malmström13O. Wallner14I. Boldogh15T. Helleday16C. Kalderén17A. Egesten18Respiratory Medicine, Allergology, & Palliative Medicine, Department of Clinical Sciences Lund, Lund University and Skåne University HospitalRespiratory Medicine, Allergology, & Palliative Medicine, Department of Clinical Sciences Lund, Lund University and Skåne University HospitalRespiratory Medicine, Allergology, & Palliative Medicine, Department of Clinical Sciences Lund, Lund University and Skåne University HospitalDivision of Infection Medicine, Department of Clinical Sciences, Lund UniversityDivision of Infection Medicine, Department of Clinical Sciences, Lund UniversityDivision of Infection Medicine, Department of Clinical Sciences, Lund UniversityDepartment of Microbiology and Immunology, University of Texas Medical Branch at GalvestonDivision of Airway Inflammation, Department of Experimental Medical Sciences, Lund UniversityRespiratory Medicine, Allergology, & Palliative Medicine, Department of Clinical Sciences Lund, Lund University and Skåne University HospitalDepartment of Microbiology and Immunology, University of Texas Medical Branch at GalvestonRespiratory Cell Biology, Department of Experimental Medical Sciences Lund, Lund UniversityScience for Life Laboratory, Department of Oncology-Pathology, Karolinska InstitutetDivision of Airway Inflammation, Department of Experimental Medical Sciences, Lund UniversityDivision of Infection Medicine, Department of Clinical Sciences, Lund UniversityScience for Life Laboratory, Department of Oncology-Pathology, Karolinska InstitutetDepartment of Microbiology and Immunology, University of Texas Medical Branch at GalvestonScience for Life Laboratory, Department of Oncology-Pathology, Karolinska InstitutetScience for Life Laboratory, Department of Oncology-Pathology, Karolinska InstitutetRespiratory Medicine, Allergology, & Palliative Medicine, Department of Clinical Sciences Lund, Lund University and Skåne University HospitalIdiopathic pulmonary fibrosis is a disease caused by persistent micro-injuries to the lung ultimately resulting in death. Here, the authors describe the use of a small molecule OGG1 inhibitor, TH5487, as a potent and potentially clinically relevant treatment for IPF.https://doi.org/10.1038/s41467-023-36314-5 |
spellingShingle | L. Tanner A. B. Single R. K. V. Bhongir M. Heusel T. Mohanty C. A. Q. Karlsson L. Pan C-M. Clausson J. Bergwik K. Wang C. K. Andersson R. M. Oommen J. S. Erjefält J. Malmström O. Wallner I. Boldogh T. Helleday C. Kalderén A. Egesten Small-molecule-mediated OGG1 inhibition attenuates pulmonary inflammation and lung fibrosis in a murine lung fibrosis model Nature Communications |
title | Small-molecule-mediated OGG1 inhibition attenuates pulmonary inflammation and lung fibrosis in a murine lung fibrosis model |
title_full | Small-molecule-mediated OGG1 inhibition attenuates pulmonary inflammation and lung fibrosis in a murine lung fibrosis model |
title_fullStr | Small-molecule-mediated OGG1 inhibition attenuates pulmonary inflammation and lung fibrosis in a murine lung fibrosis model |
title_full_unstemmed | Small-molecule-mediated OGG1 inhibition attenuates pulmonary inflammation and lung fibrosis in a murine lung fibrosis model |
title_short | Small-molecule-mediated OGG1 inhibition attenuates pulmonary inflammation and lung fibrosis in a murine lung fibrosis model |
title_sort | small molecule mediated ogg1 inhibition attenuates pulmonary inflammation and lung fibrosis in a murine lung fibrosis model |
url | https://doi.org/10.1038/s41467-023-36314-5 |
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