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Nutrients and Metabolites as Signalling Molecules in Osteoclasts.
Kavishadhi Chandrasekaran1,2, Sitao Hu1, Kara Farstad-O'Halloran1
1School of Biomedical Sciences, University of Western Australia, Perth, WA, 6009, Australia.
Current Osteoporosis Reports
|February 9, 2026
Summary
Nutrients and metabolites are key signaling molecules regulating osteoclast function. Understanding these metabolic pathways offers new therapeutic targets for bone diseases.
Area of Science:
- Cell Biology
- Metabolism
- Immunology
Background:
- Osteoclast differentiation and function are primarily studied through genetic and transcriptional pathways.
- The role of cellular metabolism and nutrient-sensing mechanisms in osteoclasts is an emerging area of research.
- Metabolites are increasingly recognized as crucial signaling molecules beyond their roles in energy production or biosynthesis.
Purpose of the Study:
- To review the concept of nutrients and metabolites as instructive signaling molecules in osteoclasts.
- To categorize key metabolites based on their signaling roles.
- To examine how metabolites influence osteoclastogenesis via metabolic, epigenetic, and inflammatory pathways.
Main Methods:
- Literature review of recent studies on nutrient metabolism in osteoclasts.
- Categorization of metabolites based on their signaling functions.
- Analysis of pathways including metabolic, epigenetic, and inflammatory influences.
Main Results:
- Nutrients (glucose, amino acids, lipids) and metabolites (succinate, itaconate, αKG, SAM, acetyl-CoA) regulate osteoclast formation and function.
- These molecules modulate signaling cascades, epigenetic landscapes, and inflammatory responses.
- Metabolites interact with nutrient sensors (aldolase, mTORC1, CPT1) and transcriptional regulators (NFATc1, PPARs).
Conclusions:
- Osteoclast metabolism is intrinsically linked to cellular fate via nutrient-sensing and metabolite-driven signaling.
- Elucidating these metabolic pathways is crucial for understanding osteoclast regulation.
- Identifying these pathways may lead to novel metabolic therapeutic targets for bone diseases.
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