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Epigenetic regulation of bone mass

Epigenetic regulation of bone mass
Epigenetic regulation of bone mass
Osteoporosis, characterised by low bone mass, poor bone structure, and an increased risk of fracture, is a major public health problem. There is increasing evidence that the influence of the environment on gene expression, through epigenetic processes, contributes to variation in BMD and fracture risk across the lifecourse. Such epigenetic processes include DNA methylation, histone and chromatin modifications and non-coding RNAs. Examples of associations with phenotype include DNA methylation in utero linked to maternal vitamin D status, and to methylation of target genes such as OPG and RANKL being associated with osteoporosis in later life. Epigenome-wide association studies and multi-omics technologies have further revealed susceptibility loci, and histone acetyltransferases, deacetylases and methylases are being considered as therapeutic targets. This review encompasses recent advances in our understanding of epigenetic mechanisms in the regulation of bone mass and osteoporosis development, and outlines possible diagnostic and prognostic biomarker applications.
DNA methylation, bone, development, epidemiology, epigenetics, osteoporosis
1521-690X
Curtis, Elizabeth
12aba0c3-1e9e-49ef-a7e9-3247e649cdd6
Fuggle, Nicholas
9ab0c81a-ac67-41c4-8860-23e0fdb1a900
Cooper, Cyrus
e05f5612-b493-4273-9b71-9e0ce32bdad6
Harvey, Nicholas
ce487fb4-d360-4aac-9d17-9466d6cba145
Curtis, Elizabeth
12aba0c3-1e9e-49ef-a7e9-3247e649cdd6
Fuggle, Nicholas
9ab0c81a-ac67-41c4-8860-23e0fdb1a900
Cooper, Cyrus
e05f5612-b493-4273-9b71-9e0ce32bdad6
Harvey, Nicholas
ce487fb4-d360-4aac-9d17-9466d6cba145

Curtis, Elizabeth, Fuggle, Nicholas, Cooper, Cyrus and Harvey, Nicholas (2022) Epigenetic regulation of bone mass. Best Practice & Research Clinical Endocrinology & Metabolism, 36 (2), [101612]. (doi:10.1016/j.beem.2021.101612).

Record type: Article

Abstract

Osteoporosis, characterised by low bone mass, poor bone structure, and an increased risk of fracture, is a major public health problem. There is increasing evidence that the influence of the environment on gene expression, through epigenetic processes, contributes to variation in BMD and fracture risk across the lifecourse. Such epigenetic processes include DNA methylation, histone and chromatin modifications and non-coding RNAs. Examples of associations with phenotype include DNA methylation in utero linked to maternal vitamin D status, and to methylation of target genes such as OPG and RANKL being associated with osteoporosis in later life. Epigenome-wide association studies and multi-omics technologies have further revealed susceptibility loci, and histone acetyltransferases, deacetylases and methylases are being considered as therapeutic targets. This review encompasses recent advances in our understanding of epigenetic mechanisms in the regulation of bone mass and osteoporosis development, and outlines possible diagnostic and prognostic biomarker applications.

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Epigenetic Regulation of Bone Mass 2021_11_24 R1 noEN - Accepted Manuscript
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Accepted/In Press date: 1 January 2022
e-pub ahead of print date: 4 January 2022
Published date: March 2022
Additional Information: Funding Information: We would like to thank the UK Medical Research Council (MC_PC_21003; MC_PC_21001), National Institute for Health Research, Wellcome Trust, Versus Arthritis, Royal Osteoporosis Society (ROS Osteoporosis and Bone Research Academy) and International Osteoporosis Foundation for supporting this work. This article adapts, with permission, text from our previous work [ 6 , 19 , 85 ]. Funding Information: EMC has been supported by an NIHR Clinical Lectureship , NRF is supported by a Dunhill Trust Clinical Research Fellowship. These funders had no role in this article. Publisher Copyright: © 2021 Elsevier Ltd
Keywords: DNA methylation, bone, development, epidemiology, epigenetics, osteoporosis

Identifiers

Local EPrints ID: 454931
URI: http://eprints.soton.ac.uk/id/eprint/454931
ISSN: 1521-690X
PURE UUID: 3a37fe5f-e7f3-481c-b28e-72919e6141b1
ORCID for Elizabeth Curtis: ORCID iD orcid.org/0000-0002-5147-0550
ORCID for Cyrus Cooper: ORCID iD orcid.org/0000-0003-3510-0709
ORCID for Nicholas Harvey: ORCID iD orcid.org/0000-0002-8194-2512

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Date deposited: 01 Mar 2022 17:51
Last modified: 01 Jan 2023 05:01

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