000			01793 am a22002293u 4500
042			_adc
100	1	0	_aCurtis, Elizabeth M _eauthor
700	1	0	_aFuggle, Nicholas R _eauthor _92542
700	1	0	_aCooper, Cyrus _eauthor
700	1	0	_aHarvey, Nicholas C _eauthor
245	0	0	_aBest Practice Research Clinical Endocrinology and Metabolism Epigenetic Regulation of Bone Mass
260			_c2022-03-01.
500			_a/pmc/articles/PMC7614112/
500			_a/pubmed/35120798
520			_aOsteoporosis, 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.
540			_a
546			_aen
690			_aArticle
655	7		_aText _2local
786	0		_nBest Pract Res Clin Endocrinol Metab
856	4	1	_uhttp://dx.doi.org/10.1016/j.beem.2021.101612 _zConnect to this object online.
999			_c2009 _d2009