ReviewFrontiers in endocrinology2024
Citrate: a key signalling molecule and therapeutic target for bone remodeling disorder.
Review in Frontiers in endocrinology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Metabolism of citrate-mediated PI3K-Akt signaling and primary cilium regulates spatiotemporal craniofacial mineralization.Bioactive materials · 2026Article
- Targeting the osteoporotic bone microenvironment: Mechanistic insight and therapeutic biomaterials for accelerating bone regeneration.Bioactive materials · 2026Review
- Discovery and Characterization of a Nonacidic Small-Molecule Inhibitor of the Sodium-Coupled Dicarboxylate Transporter NaCT.Journal of medicinal chemistry · 2026Article
- Metabolic signatures in osteoporotic cancellous bone: a comprehensive dual-platform metabolomic analysis.BMC musculoskeletal disorders · 2025Article
- Accelerated osteocytic citrate production in chronic kidney disease is associated with protection of the kidney.bioRxiv : the preprint server for biology · 2025Article
- A Collagen Membrane Pretreated with Citrate Promotes Collagen Mineralization and Bone Regeneration.Journal of functional biomaterials · 2025Article
- Bone marrow mesenchymal stem cells and adipocytes in haematological malignancies.Oncology reviews · 2025Article
- Lactylation-related geneFrontiers in immunology · 2025Article
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5 authors.
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Abstract
Bone remodeling is a continuous cyclic process that maintains and regulates bone structure and strength. The disturbance of bone remodeling leads to a series of bone metabolic diseases. Recent studies have shown that citrate, an intermediate metabolite of the tricarboxylic acid (TCA) cycle, plays an important role in bone remodeling. But the exact mechanism is still unclear. In this study, we focused on the systemic regulatory mechanism of citrate on bone remodeling, and found that citrate is involved in bone remodeling in multiple ways. The participation of citrate in oxidative phosphorylation (OXPHOS) facilitates the generation of ATP, thereby providing substantial energy for bone formation and resorption. Osteoclast-mediated bone resorption releases citrate from bone mineral salts, which is subsequently released as an energy source to activate the osteogenic differentiation of stem cells. Finally, the differentiated osteoblasts secrete into the bone matrix and participate in bone mineral salts formation. As a substrate of histone acetylation, citrate regulates the expression of genes related to bone formation and bone reabsorption. Citrate is also a key intermediate in the metabolism and synthesis of glucose, fatty acids and amino acids, which are three major nutrients in the organism. Citrate can also be used as a biomarker to monitor bone mass transformation and plays an important role in the diagnosis and therapeutic evaluation of bone remodeling disorders. Citrate imbalance due to citrate transporter could result in the supression of osteoblast/OC function through histone acetylation, thereby contributing to disorders in bone remodeling. Therefore, designing drugs targeting citrate-related proteins to regulate bone citrate content provides a new direction for the drug treatment of diseases related to bone remodeling disorders.
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