Osteocytic oxygen sensing controls bone mass through epigenetic regulation of sclerostin
Osteocytes reside in a low oxygen environment, but it is not clear if oxygen sensing regulates their function. Here, the authors show that deletion of the oxygen sensor prolyl hydroxylase 2 in osteocytes leads to increased bone mass via regulation of sclerostin, and reduces bone loss in mouse models...
Main Authors: | , , , , , , |
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Format: | Article |
Language: | English |
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Nature Portfolio
2018-07-01
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Series: | Nature Communications |
Online Access: | https://doi.org/10.1038/s41467-018-04679-7 |
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author | Steve Stegen Ingrid Stockmans Karen Moermans Bernard Thienpont Patrick H. Maxwell Peter Carmeliet Geert Carmeliet |
author_facet | Steve Stegen Ingrid Stockmans Karen Moermans Bernard Thienpont Patrick H. Maxwell Peter Carmeliet Geert Carmeliet |
author_sort | Steve Stegen |
collection | DOAJ |
description | Osteocytes reside in a low oxygen environment, but it is not clear if oxygen sensing regulates their function. Here, the authors show that deletion of the oxygen sensor prolyl hydroxylase 2 in osteocytes leads to increased bone mass via regulation of sclerostin, and reduces bone loss in mouse models of osteoporosis. |
first_indexed | 2024-12-19T05:11:17Z |
format | Article |
id | doaj.art-a2f76a4ad04d47d2b0409ff2a91de740 |
institution | Directory Open Access Journal |
issn | 2041-1723 |
language | English |
last_indexed | 2024-12-19T05:11:17Z |
publishDate | 2018-07-01 |
publisher | Nature Portfolio |
record_format | Article |
series | Nature Communications |
spelling | doaj.art-a2f76a4ad04d47d2b0409ff2a91de7402022-12-21T20:34:48ZengNature PortfolioNature Communications2041-17232018-07-019111610.1038/s41467-018-04679-7Osteocytic oxygen sensing controls bone mass through epigenetic regulation of sclerostinSteve Stegen0Ingrid Stockmans1Karen Moermans2Bernard Thienpont3Patrick H. Maxwell4Peter Carmeliet5Geert Carmeliet6Laboratory of Clinical and Experimental Endocrinology, Department of Chronic Diseases, Metabolism and Ageing, KU LeuvenLaboratory of Clinical and Experimental Endocrinology, Department of Chronic Diseases, Metabolism and Ageing, KU LeuvenLaboratory of Clinical and Experimental Endocrinology, Department of Chronic Diseases, Metabolism and Ageing, KU LeuvenLaboratory for Functional Epigenetics, Department of Human Genetics, KU LeuvenCambridge Institute for Medical Research, University of CambridgeLaboratory of Angiogenesis and Vascular Metabolism, Center for Cancer Biology, Department of Oncology, KU LeuvenLaboratory of Clinical and Experimental Endocrinology, Department of Chronic Diseases, Metabolism and Ageing, KU LeuvenOsteocytes reside in a low oxygen environment, but it is not clear if oxygen sensing regulates their function. Here, the authors show that deletion of the oxygen sensor prolyl hydroxylase 2 in osteocytes leads to increased bone mass via regulation of sclerostin, and reduces bone loss in mouse models of osteoporosis.https://doi.org/10.1038/s41467-018-04679-7 |
spellingShingle | Steve Stegen Ingrid Stockmans Karen Moermans Bernard Thienpont Patrick H. Maxwell Peter Carmeliet Geert Carmeliet Osteocytic oxygen sensing controls bone mass through epigenetic regulation of sclerostin Nature Communications |
title | Osteocytic oxygen sensing controls bone mass through epigenetic regulation of sclerostin |
title_full | Osteocytic oxygen sensing controls bone mass through epigenetic regulation of sclerostin |
title_fullStr | Osteocytic oxygen sensing controls bone mass through epigenetic regulation of sclerostin |
title_full_unstemmed | Osteocytic oxygen sensing controls bone mass through epigenetic regulation of sclerostin |
title_short | Osteocytic oxygen sensing controls bone mass through epigenetic regulation of sclerostin |
title_sort | osteocytic oxygen sensing controls bone mass through epigenetic regulation of sclerostin |
url | https://doi.org/10.1038/s41467-018-04679-7 |
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