ReviewCell biochemistry and function2026
Epigenetic Regulation of Bone Homeostasis in Osteoporosis: Mechanisms, Evidence Gaps, and Translational Prospects.
Review in Cell biochemistry and function, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
Osteoporosis arises from an imbalance among osteoblast-mediated bone formation, osteoclast-mediated bone resorption, and osteocyte-directed mechanosensory control, but the molecular events that connect aging, hormonal change, inflammation, and mechanical unloading to bone loss remain incompletely resolved. Epigenetic mechanisms, including DNA methylation, histone modifications, non-coding RNAs (ncRNAs), and RNA modifications, provide one route through which environmental and cellular signals reshape bone-cell function. This review summarizes current evidence linking epigenetic regulation to osteoblasts, osteoclasts, and osteocytes; distinguishes human, animal, and in vitro evidence; and evaluates the translational maturity of proposed biomarkers and therapies. DNA methylation and histone modifications have strong mechanistic support in bone-cell differentiation models, whereas ncRNA and N6-methyladenosine (m6A) pathways are expanding rapidly but remain largely preclinical. Blood-based methylation or RNA signatures and epigenetic therapies are promising but should be considered exploratory until validated in prospective cohorts, fracture-related endpoints, and bone-cell-specific intervention studies.
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