Targeting cyclin-dependent kinases for the treatment of pulmonary arterial hypertension
Cells of the pulmonary vasculature show a hyperproliferative phenotype in pulmonary arterial hypertension (PAH), thus contributing to the disease pathogenesis. Here the authors show that cyclin-dependent kinases are overactivated in PAH, and that their pharmacological inhibition attenuates the disea...
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2019-05-01
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doaj-4090a81f202846ada6a47e71478ee8362021-05-11T11:30:43ZengNature Publishing GroupNature Communications2041-17232019-05-0110111710.1038/s41467-019-10135-xTargeting cyclin-dependent kinases for the treatment of pulmonary arterial hypertensionAstrid Weiss0Moritz Christian Neubauer1Dinesh Yerabolu2Baktybek Kojonazarov3Beate Christiane Schlueter4Lavinia Neubert5Danny Jonigk6Nelli Baal7Clemens Ruppert8Peter Dorfmuller9Soni Savai Pullamsetti10Norbert Weissmann11Hossein-Ardeschir Ghofrani12Friedrich Grimminger13Werner Seeger14Ralph Theo Schermuly15Justus-Liebig-University Giessen (JLU)Justus-Liebig-University Giessen (JLU)Justus-Liebig-University Giessen (JLU)Justus-Liebig-University Giessen (JLU)Justus-Liebig-University Giessen (JLU)Member of the German Center for Lung Research (DZL)Member of the German Center for Lung Research (DZL)Justus-Liebig-University Giessen (JLU)Justus-Liebig-University Giessen (JLU)Member of the German Center for Lung Research (DZL)Universities of Giessen and Marburg Lung Center (UGMLC)Justus-Liebig-University Giessen (JLU)Justus-Liebig-University Giessen (JLU)Justus-Liebig-University Giessen (JLU)Justus-Liebig-University Giessen (JLU)Justus-Liebig-University Giessen (JLU)Cells of the pulmonary vasculature show a hyperproliferative phenotype in pulmonary arterial hypertension (PAH), thus contributing to the disease pathogenesis. Here the authors show that cyclin-dependent kinases are overactivated in PAH, and that their pharmacological inhibition attenuates the disease in two independent rodent modelshttps://doi.org/10.1038/s41467-019-10135-x |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Astrid Weiss Moritz Christian Neubauer Dinesh Yerabolu Baktybek Kojonazarov Beate Christiane Schlueter Lavinia Neubert Danny Jonigk Nelli Baal Clemens Ruppert Peter Dorfmuller Soni Savai Pullamsetti Norbert Weissmann Hossein-Ardeschir Ghofrani Friedrich Grimminger Werner Seeger Ralph Theo Schermuly |
spellingShingle |
Astrid Weiss Moritz Christian Neubauer Dinesh Yerabolu Baktybek Kojonazarov Beate Christiane Schlueter Lavinia Neubert Danny Jonigk Nelli Baal Clemens Ruppert Peter Dorfmuller Soni Savai Pullamsetti Norbert Weissmann Hossein-Ardeschir Ghofrani Friedrich Grimminger Werner Seeger Ralph Theo Schermuly Targeting cyclin-dependent kinases for the treatment of pulmonary arterial hypertension Nature Communications |
author_facet |
Astrid Weiss Moritz Christian Neubauer Dinesh Yerabolu Baktybek Kojonazarov Beate Christiane Schlueter Lavinia Neubert Danny Jonigk Nelli Baal Clemens Ruppert Peter Dorfmuller Soni Savai Pullamsetti Norbert Weissmann Hossein-Ardeschir Ghofrani Friedrich Grimminger Werner Seeger Ralph Theo Schermuly |
author_sort |
Astrid Weiss |
title |
Targeting cyclin-dependent kinases for the treatment of pulmonary arterial hypertension |
title_short |
Targeting cyclin-dependent kinases for the treatment of pulmonary arterial hypertension |
title_full |
Targeting cyclin-dependent kinases for the treatment of pulmonary arterial hypertension |
title_fullStr |
Targeting cyclin-dependent kinases for the treatment of pulmonary arterial hypertension |
title_full_unstemmed |
Targeting cyclin-dependent kinases for the treatment of pulmonary arterial hypertension |
title_sort |
targeting cyclin-dependent kinases for the treatment of pulmonary arterial hypertension |
publisher |
Nature Publishing Group |
series |
Nature Communications |
issn |
2041-1723 |
publishDate |
2019-05-01 |
description |
Cells of the pulmonary vasculature show a hyperproliferative phenotype in pulmonary arterial hypertension (PAH), thus contributing to the disease pathogenesis. Here the authors show that cyclin-dependent kinases are overactivated in PAH, and that their pharmacological inhibition attenuates the disease in two independent rodent models |
url |
https://doi.org/10.1038/s41467-019-10135-x |
work_keys_str_mv |
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