Rheumatology · 17 h ago
Review examines post-translational control of bone homeostasis
A review in BMC Medicine summarizes how post-translational modifications interact with cellular signaling in bone-forming, bone-resorbing and bone-sensing cells. The authors discuss links to skeletal diseases and highlight gaps in evidence, including uncertainty about the causal role of many specific modifications.
- PTMs may modify signaling in multiple bone cell types.
- Dysregulated PTMs are linked to several skeletal diseases.
- Causal evidence remains unclear for many specific PTM events.
- New multi-omics methods may help fill evidence gaps.
Bone homeostasis depends on coordinated activity among osteoblasts, osteoclasts, osteocytes and their microenvironment. This review summarizes evidence on how post-translational modifications (PTMs) regulate proteins involved in these cells’ functions, alongside transcriptional programs and established signaling pathways.
The authors organize the literature around interactions between PTMs and signaling, PTM-mediated signal gating or amplification, and regulation across cell types, cellular compartments, developmental and aging stages, and disease states. They describe associations between dysregulated PTMs and osteoporosis, osteoarthritis, metabolic and inflammatory bone diseases, and impaired bone repair.
The review notes that evidence is uneven across PTM types and skeletal cell populations, and that causal roles for many site-specific events remain unclear. Quantitative PTM proteomics, single-cell and spatial analyses, and multi-omics approaches may help address these gaps. The article synthesizes mechanistic research rather than reporting a clinical study, and it does not establish treatment implications or support changes to clinical practice.
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BMC Medicine: Networked control of bone homeostasis: interfacing post-translational modifications with cellular signaling ↗This is an automated AI-condensed summary that has not yet been reviewed by an editor. Always consult the full item at the original source.