ReviewCurrent osteoporosis reports2026
Nutrients and Metabolites as Signalling Molecules in Osteoclasts.
Review in Current osteoporosis reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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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Who cites it
3 citing papers in PubMed.
- ACOD1 deficiency promotes DDX1 methylation-mediated mitochondrial dysfunction and dermal papilla cell senescence in androgenetic alopecia.BMC medicine · 2026Article
- Tumor-associated osteoclasts converge on a matrix-sulfation program across human bone tumors.Frontiers in cell and developmental biology · 2026Article
- High-protein golden sea cucumber jelly candy as a nutritional innovation to enhance dental and jaw development in children with childhood malnutrition (1-5 years): Evidence from an experimental Wistar rat model.Journal of advanced veterinary and animal research · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of reviewThis review aims to highlight the emerging concept that nutrients and metabolites act not merely as energy sources or biosynthetic precursors, but also as instructive signalling molecules in osteoclasts. While much is known about transcriptional and genetic pathways governing osteoclast differentiation and function, comparatively little attention has been given to the role of cellular metabolism and nutrient-sensing mechanisms. This review seeks to categorise key metabolites based on their signalling roles and examine how they influence osteoclastogenesis through metabolic, epigenetic, and inflammatory pathways. RECENT
findingsRecent studies have demonstrated that nutrients such as glucose, amino acids, and lipids, along with their intermediary metabolites such as succinate, itaconate, α-ketoglutarate (αKG), S-adenosylmethionine (SAM), and acetyl-CoA, regulate osteoclast formation and function by modulating signalling cascades and epigenetic landscapes. These molecules engage nutrient sensors (e.g., aldolase, mTORC1, CPT1) and transcriptional regulators (e.g., NFATc1, PPARs), while also affecting chromatin structure, inflammatory responses, and organelle dynamics. Osteoclast metabolism is tightly linked to cellular fate through nutrient-sensing and metabolite-driven signalling. Elucidating these pathways will reshape our understanding of osteoclast regulation and help identify new metabolic targets for treating bone diseases.
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Registered trials
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