Direct and indirect regulation of bone metabolism by lactoferrin
Wu Y., Zhang C., Lv C.
Narrative Review, published in Front Endocrinol (Lausanne) (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Narrative Review
- Journal
- Front Endocrinol (Lausanne) (2025)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 41169473
- PMCID
- PMC12568430
- DOI
- 10.3389/fendo.2025.1660312
- Citations
- 1
Abstract (original English)
Lactoferrin exerts positive regulation on bone metabolism through both direct and indirect pathways. Directly, it modulates osteoblasts, osteoclasts, and chondrocytes via factors such as insulin-like growth factor (IGF), low-density lipoprotein receptor-associated protein (LRP), transforming growth factor β (TGF-β) receptor, and bone morphogenetic proteins (BMPs). These factors promote differentiation and inhibit apoptosis of bone metabolism-related cells through signaling pathways including the receptor activator of nuclear factor kappa-B (RANK), its ligand RANKL, and osteoprotegerin (OPG), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK), macrophage colony-stimulating factor (M-CSF), Ca2+, phosphoinositide 3-kinase/protein kinase B (PI3K/Akt), Wnt/β-catenin, BMP-2/Smad, and TGF-β. Indirectly, lactoferrin influences skeletal muscle, energy metabolism, intestinal microbiota, immune function, and calcium-phosphorus homeostasis, all of which positively affect bone metabolism. In-depth research into lactoferrin-derived peptides and their complexes for slow-release systems may open new avenues for treating orthopedic diseases. However, the mechanisms by which lactoferrin regulates bone metabolism remain incompletely understood. This review aims to summarize these mechanisms and
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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