Nicotinamide as a therapeutic agent for bone diseases
3
조회
0
다운로드
0
인용
0
참고문헌
키워드
초록
Nicotinamide (NAM), a water-soluble derivative of vitamin B3, has emerged as a potential therapeutic agent for bonerelated disorders. In particular, it promotes bone metabolism and alleviates delayed tooth eruptions associated with cleidocranial dysplasia (CCD). NAM serves as a precursor for nicotinamide adenine dinucleotide, a key coenzyme involved in cellular metabolism that plays an essential role in oxidative phosphorylation and mitochondrial function. Recent research has highlighted the capacity of NAM to enhance osteogenic differentiation and regulate the interaction between osteoblasts and osteoclasts, which is critical for maintaining bone homeostasis. Moreover, the effect of NAM in preventing delayed tooth eruptions in CCD models underscores its potential as a noninvasive therapeutic option. Considering its safety profile and therapeutic potential, NAM is a promising candidate for longterm treatment of bone diseases and prevention of age-related bone disorders.
Abstract
Nicotinamide (NAM), a water-soluble derivative of vitamin B3, has emerged as a potential therapeutic agent for bonerelated disorders. In particular, it promotes bone metabolism and alleviates delayed tooth eruptions associated with cleidocranial dysplasia (CCD). NAM serves as a precursor for nicotinamide adenine dinucleotide, a key coenzyme involved in cellular metabolism that plays an essential role in oxidative phosphorylation and mitochondrial function. Recent research has highlighted the capacity of NAM to enhance osteogenic differentiation and regulate the interaction between osteoblasts and osteoclasts, which is critical for maintaining bone homeostasis. Moreover, the effect of NAM in preventing delayed tooth eruptions in CCD models underscores its potential as a noninvasive therapeutic option. Considering its safety profile and therapeutic potential, NAM is a promising candidate for longterm treatment of bone diseases and prevention of age-related bone disorders.
참고문헌 (49)
- Rolfe HM, "A review of nicotinamide : treatment of skin diseases and potential side effects", J Cosmet Dermatol, 13, pp.324~328 (2014)[DOI]
- Chen AC, "A phase 3 randomized trial of nicotinamide for skin-cancer chemoprevention", N Engl J Med, 373, pp.1618~1626 (2015)[DOI]
- Iqbal T, "The therapeutic perspective of NAD+precursors in age-related diseases", Biochem Biophys Res Commun, 702, pp.149590~ (2024)[DOI]
- Srivastava S, "Emerging therapeutic roles for NAD+ metabolism in mitochondrial and age-related disorders", Clin Transl Med, 5, pp.25~ (2016)[DOI]
- Mitchell SJ, "Nicotinamide improves aspects of healthspan, but not lifespan, in mice", Cell Metab, 27, pp.667~676 (2018)[DOI]
- Imai S, "Transcriptional silencing and longevity protein Sir2 is an NAD-dependent histone deacetylase", Nature, 403, pp.795~800 (2000)[DOI]
- Avalos JL, "Mechanism of sirtuin inhibition by nicotinamide : altering the NAD+ cosubstrate specificity of a Sir2 enzyme", Mol Cell, 17, pp.855~868 (2005)[DOI]
- Hwang ES, "Nicotinamide is an inhibitor of SIRT1 in vitro, but can be a stimulator in cells", Cell Mol Life Sci, 74, pp.3347~3362 (2017)[DOI]
- Meng Y, "Nicotinamide promotes cell survival and differentiation as kinase inhibitor in human pluripotent stem cells", Stem Cell Reports, 11, pp.1347~1356 (2018)[DOI]
- Ma L, "SIRT1 and SIRT2 inhibition impairs pediatric soft tissue sarcoma growth", Cell Death Dis, 5, pp.e1483~ (2014)[DOI]
- Hill LJ, "Meat intake and the dose of vitamin B3-nicotinamide : cause of the causes of disease transitions, health divides, and health futures?", Int J Tryptophan Res, 10, pp.1178646917704662~ (2017)[DOI]
- Hołubiec P, "Pathophysiology and clinical management of pellagra-a review", Folia Med Cracov, 61, pp.125~137 (2021)[DOI]
- Kaymak Y, "An investigation of efficacy of topical niacinamide for the treatment of mild and moderate acne vulgaris", J Turk Acad Dermatol, 2, pp.jtad82402a~ (2008)
- Hakozaki T, "The effect of niacinamide on reducing cutaneous pigmentation and suppression of melanosome transfer", Br J Dermatol, 147, pp.20~31 (2002)[DOI]
- Soma Y, "Moisturizing effects of topical nicotinamide on atopic dry skin", Int J Dermatol, 44, pp.197~202 (2005)[DOI]
- Elliott RB, "A population based strategy to prevent insulin-dependent diabetes using nicotinamide", J Pediatr Endocrinol Metab, 9, pp.501~509 (1996)[DOI]
- Yoon H, "Nicotinamide improves delayed tooth eruption in Runx2+", -mice, 2021, pp.100, 423~431
- Damian DL, "Nicotinamide for skin cancer chemoprevention", Australas J Dermatol, 58, pp.174~180 (2017)[DOI]
- Wise GE, "Mechanisms of tooth eruption and orthodontic tooth movement", J Dent Res, 87, pp.414~434 (2008)[DOI]
- Heinrich J, "CSF-1, RANKL and OPG regulate osteoclastogenesis during murine tooth eruption", Arch Oral Biol, 50, pp.897~908 (2005)[DOI]
- Ida-Yonemochi H, "Disturbed tooth eruption in osteopetrotic(op", op)mice : histopathogenesis of tooth malformation and odontomas, 2002, pp.31, 361~373
- Sheng ZF, "OPG knockout mouse teeth display reduced alveolar bone mass and hypermineralization in enamel and dentin", Arch Oral Biol, 55, pp.288~293 (2010)[DOI]
- Boyce BF, "Functions of RANKL", RANK, Arch Biochem Biophys, pp.2008, 473[DOI]
- Sai Charan KV, "The tooth eruption and its abnormalities-a narrative review", SRM J Res Dent Sci, 13, pp.109~114 (2022)[DOI]
- Suri L, "Delayed tooth eruption : pathogenesis, diagnosis, and treatment. A literature review", Am J Orthod Dentofacial Orthop, 126, pp.432~445 (2004)[DOI]
- Ray JG, "Noneruption of teeth in amelogenesis imperfecta : a report of two cases and review", J Oral Maxillofac Pathol, 26, pp.254~258 (2022)[DOI]
- Kaloust S, "Dental development in Apert syndrome", Cleft Palate Craniofac J, 34, pp.117~121 (1997)[DOI]
- Kreiborg S, "Tooth formation and eruption-lessons learnt from cleidocranial dysplasia", Eur J Oral Sci, 126(Suppl 1), pp.72~80 (2018)[DOI]
- Canger EM, "Amelogenesis imperfecta, hypoplastic type associated with some dental abnormalities : a case report", Braz Dent J, 21, pp.170~174 (2010)[DOI]
- Hohoff A, "The spectrum of Apert syndrome : phenotype, particularities in orthodontic treatment, and characteristics of orthognathic surgery", Head Face Med, 3, pp.10~ (2007)[DOI]
- Kim HJ, "Post-translational regulations of transcriptional activity of RUNX2", Mol Cells, 43, pp.160~167 (2020)[DOI]
- Ryoo HM, "RUNX2 mutations in cleidocranial dysplasia patients", Oral Dis, 16, pp.55~60 (2010)[DOI]
- Kim WJ, "RUNX2-modifying enzymes : therapeutic targets for bone diseases", Exp Mol Med, 52, pp.1178~1184 (2020)[DOI]
- Barth FA, "Therapeutic protocol for orthosurgical management of class III malocclusion in patients with cleidocranial dysostosis", J Craniofac Surg, 29, pp.1642~1647 (2018)[DOI]
- Roberts T, "Cleidocranial dysplasia : a review of the dental, historical, and practical implications with an overview of the South African experience", Oral Surg Oral Med Oral Pathol Oral Radiol, 115, pp.46~55 (2013)[DOI]
- Yoda S, "Delayed tooth eruption and suppressed osteoclast number in the eruption pathway of heterozygous Runx2", Cbfa1 knockout mice, 2004, pp.49, 435~442
- Martínez-Reyes I, "Mitochondrial TCA cycle metabolites control physiology and disease", Nat Commun, 11, pp.102~ (2020)[DOI]
- Suh J, "Mitochondrial fragmentation and donut formation enhance mitochondrial secretion to promote osteogenesis", Cell Metab, 35, pp.345~360 (2023)[DOI]
- Yoon H, "Nicotinamide enhances osteoblast differentiation through activation of the mitochondrial antioxidant defense system", Exp Mol Med, 55, pp.1531~1543 (2023)[DOI]
- Kim HJ, "ROS-induced PADI2downregulation accelerates cellular senescence via the stimulation of SASP production and NFκB activation", Cell Mol Life Sci, 79, pp.155~ (2022)[DOI]
- Verdin E, "NAD+ in aging, metabolism, and neurodegeneration", Science, 350, pp.1208~1213 (2015)[DOI]
- Covarrubias AJ, "NAD+ metabolism and its roles in cellular processes during ageing", Nat Rev Mol Cell Biol, 22, pp.119~141 (2021)[DOI]
- Song J, "Nicotinamide mononucleotide promotes osteogenesis and reduces adipogenesis by regulating mesenchymal stromal cells via the SIRT1 pathway in aged bone marrow", Cell Death Dis, 10, pp.336~ (2019)[DOI]
- Liang H, "Nicotinamide mononucleotide alleviates Aluminum induced bone loss by inhibiting the TXNIP-NLRP3 inflammasome", Toxicol Appl Pharmacol, 362, pp.20~27 (2019)[DOI]
- Huang RX, "Nicotinamide mononucleotide attenuates glucocorticoid‑induced osteogenic inhibition by regulating the SIRT1", PGC‑1α signaling pathway, 2020, pp.22, 145~154
- Kim HN, "A decrease in NAD+ contributes to the loss of osteoprogenitors and bone mass with aging", NPJ Aging Mech Dis, 7, pp.8~ (2021)[DOI]
- Ling M, "Epigenetic regulation of Runx2 transcription and osteoblast differentiation by nicotinamide phosphoribosyltransferase", Cell Biosci, 7, pp.27~ (2017)[DOI]
- Li Y, "Nampt expression increases during osteogenic differentiation of multi-and omnipotent progenitors", Biochem Biophys Res Commun, 434, pp.117~123 (2013)[DOI]
- Hassan B, "NAMPT expression in osteoblasts controls osteoclast recruitment in alveolar bone remodeling", J Cell Physiol, 233, pp.7402~7414 (2018)[DOI]
