ArticleMolecular medicine reports2017
Nicotinamide phosphoribosyltransferase inhibits receptor activator of nuclear factor-κB ligand-induced osteoclast differentiation in vitro.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Relationship of visfatin with obesity and osteoporosis in patients with inflammatory bowel disease: a narrative review.Frontiers in immunology · 2025Review
- Visfatin Enhances RANKL-Induced Osteoclastogenesis In Vitro: Synergistic Interactions and Its Role as a Mediator in Osteoclast Differentiation and Activation.Biomolecules · 2024Article
- Beyond mechanical loading: The metabolic contribution of obesity in osteoarthritis unveils novel therapeutic targets.Heliyon · 2023Review
- Novel Adipokines and Their Role in Bone Metabolism: A Narrative Review.Biomedicines · 2023Review
- Interplay between fat cells and immune cells in bone: Impact on malignant progression and therapeutic response.Pharmacology & therapeutics · 2022Review
- Integrated Analysis of Crucial Genes and miRNAs Associated with Osteoporotic Fracture of Type 2 Diabetes.BioMed research international · 2022Article
- Association of serum levels of Visfatin, Intelectin-1, RARRES2 and their genetic variants with bone mineral density in postmenopausal females.Frontiers in endocrinology · 2022Article
- Observational
- Nicotinamide mononucleotide attenuates glucocorticoid‑induced osteogenic inhibition by regulating the SIRT1/PGC‑1α signaling pathway.Molecular medicine reports · 2020Article
- At the Crossroads of the Adipocyte and Osteoclast Differentiation Programs: Future Therapeutic Perspectives.International journal of molecular sciences · 2020Review
- Article
- Visfatin Connection: Present and Future in Osteoarthritis and Osteoporosis.Journal of clinical medicine · 2019Review
- Serum visfatin levels in patients with axial spondyloarthritis and their relationship to disease activity and spinal radiographic damage: a cross-sectional study.Rheumatology international · 2019Article
- NAMPT expression in osteoblasts controls osteoclast recruitment in alveolar bone remodeling.Journal of cellular physiology · 2018Article
- Resistin promotes the abnormal Type I collagen phenotype of subchondral bone in obese patients with end stage hip osteoarthritis.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The adipokine nicotinamide phosphoribosyltransferase (Nampt), also known as pre-B-cell colony-enhancing factor or the insulin-mimetic hormone visfatin, has a crucial role in the conversion of nicotinamide to nicotinamide mononucleotide during biosynthesis of the coenzyme nicotinamide adenine dinucleotide. Previous reports have demonstrated the inhibitory effects of Nampt on osteoclast formation from human peripheral blood mononuclear cells and CD14+ monocytes. However, the effects of Nampt on bone marrow macrophage (BMM)‑derived osteoclastogenesis and its precise role in the process remain unclear. The present in vitro study used recombinant Nampt and BMMs as osteoclast precursors demonstrated that Nampt suppresses receptor activator of nuclear factor‑κB ligand (RANKL)‑induced osteoclastogenesis by decreasing the phosphorylation of various early signal transducers, including c‑Jun N‑terminal kinase, Akt, glycogen synthase kinase‑3 β, Bruton's tyrosine kinase and phospholipase C γ‑2. In addition, western blotting and reverse transcription‑quantitative polymerase chain reaction analysis indicated that Nampt downregulates the mRNA and protein expression levels of c‑Fos and nuclear factor of activated T cells, cytoplasmic 1, leading to a decrease in the expression of osteoclast‑specific genes including tartrate‑resistant acid phosphatase, osteoclast‑associated receptor and cathepsin K. However, the bone‑resorbing activity of mature osteoclasts treated with Nampt was similar to untreated control osteoclasts. This finding indicates that Nampt exerts its anti‑osteoclastogenic activity by targeting osteoclast precursor cells rather than mature osteoclasts. Consequently, the present study demonstrated that Nampt acts as a negative regulator of RANKL‑mediated differentiation of BMMs into osteoclasts, suggesting the potential therapeutic targets to treat bone-related disorders such as osteoporosis.
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