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...

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Main Authors: Steve Stegen, Ingrid Stockmans, Karen Moermans, Bernard Thienpont, Patrick H. Maxwell, Peter Carmeliet, Geert Carmeliet
Format: Article
Language:English
Published: Nature Portfolio 2018-07-01
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.
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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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