Nicotinamide mononucleotide alleviates Aluminum induced bone loss by inhibiting the TXNIP-NLRP3 inflammasome

Liang, Hai‐Peng; Gao, Jian; Zhang, Chi; Li, Chunlin; Wang, Qi; Fan, Jinhui; Wu, Zizheng; Wang, Qiugen

doi:10.1016/j.taap.2018.10.006

Cited by 31 publications

(19 citation statements)

References 35 publications

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“…Recently, a study reported that NMN treatment improved mesenchymal stromal cells self-renewal with promoted osteogenesis and reduced adipogenesis via the SIRT1 pathway in aged and irradiated adult mice (Song et al, 2019). Moreover, NMN supplement can alleviate aluminum-induced bone injuries via suppression of the thioredoxin-interacting protein (TXNIP)-NLRP3 inflammasome pathway (Liang et al, 2019). These findings further demonstrate that NMN can be used to treat a variety of diseases involving NAD+ decline (Figure 4 and Table 1).…”

Section: Other Diseases and Improvement Of Physical Functionmentioning

confidence: 62%

“…300 mg/kg) 3 months Stimulated osteogenesis of endogenous mesenchymal stromal cells (MSCs), and protected bone from aging and irradiation induced damage in mice Song et al, 2019 AlCl 3 -treated Sprague-Dawley rats NMN (i.p. 20 mg/kg) 4 weeks Alleviated aluminum-induced bone loss Liang et al, 2019 Brain cryoinjury in Balb/c mice NMN (i.c.v. 5 mM with 7 µl) Single Protected brain in both the early and the chronic phase of cryoinjury Zhang et al, 2015 Adipocyte-specific Nampt knockout (ANKO) mice NMN (i.p.…”

Section: Human Clinical Studymentioning

confidence: 99%

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Nicotinamide Mononucleotide: A Promising Molecule for Therapy of Diverse Diseases by Targeting NAD+ Metabolism

Hong

Zhang

et al. 2020

Front. Cell Dev. Biol.

123

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NAD+, a co-enzyme involved in a great deal of biochemical reactions, has been found to be a network node of diverse biological processes. In mammalian cells, NAD+ is synthetized, predominantly through NMN, to replenish the consumption by NADase participating in physiologic processes including DNA repair, metabolism, and cell death. Correspondingly, aberrant NAD+ metabolism is observed in many diseases. In this review, we discuss how the homeostasis of NAD+ is maintained in healthy condition and provide several age-related pathological examples related with NAD+ unbalance. The sirtuins family, whose functions are NAD-dependent, is also reviewed. Administration of NMN surprisingly demonstrated amelioration of the pathological conditions in some agerelated disease mouse models. Further clinical trials have been launched to investigate the safety and benefits of NMN. The NAD+ production and consumption pathways including NMN are essential for more precise understanding and therapy of age-related pathological processes such as diabetes, ischemia-reperfusion injury, heart failure, Alzheimer's disease, and retinal degeneration.

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Section: Other Diseases and Improvement Of Physical Functionmentioning

confidence: 62%

Section: Human Clinical Studymentioning

confidence: 99%

Nicotinamide Mononucleotide: A Promising Molecule for Therapy of Diverse Diseases by Targeting NAD+ Metabolism

Hong

Zhang

et al. 2020

Front. Cell Dev. Biol.

123

View full text Add to dashboard Cite

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“…The nicotinamide mononucleotide (NMN) inhibits the expression of inflammatory factors through the TXNIP-NLRP3 inflammasome pathway, significantly reducing aluminuminduced bone damage. The knocking down of TXNIP has a similar protective effect to that of NMN in MC3T3-E1 cells [52].…”

Section: The Role Of Nlrp3 Inflammasome Activities In Bone Diseasesmentioning

confidence: 82%

The Role of NLRP3 Inflammasome Activities in Bone Diseases and Vascular Calcification

Zhang

Kuang

et al. 2020

Inflammation

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Continuous stimulation of inflammation is harmful to tissues of an organism. Inflammatory mediators not only have an effect on metabolic and inflammatory bone diseases but also have an adverse effect on certain genetic and periodontal diseases associated with bone destruction. Inflammatory factors promote vascular calcification in various diseases. Vascular calcification is a pathological process similar to bone development, and vascular diseases play an important role in the loss of bone homeostasis. The NLRP3 inflammasome is an essential component of the natural immune system. It can recognize pathogen-related molecular patterns or host-derived dangerous signaling molecules, recruit, and activate the pro-inflammatory protease caspase-1. Activated caspase-1 cleaves the precursors of IL-1β and IL-18 to produce corresponding mature cytokines or recognizes and cleaves GSDMD to mediate cell pyroptosis. In this review, we discuss the role of NLRP3 inflammasome in bone diseases and vascular calcification caused by sterile or non-sterile inflammation and explore potential treatments to prevent bone loss.

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“…NAD + is also involved in the maintenance of osteoblast differentiation, and an increase in the intracellular levels of NAD + is a necessary event for the development of senile osteoporosis. Liang et al (42) reported that nMn attenuates aluminum-induced bone loss. However, the protective effects of NAD + depletion on glucocorticoid-induced osteogenic inhibition have yet to be elucidated.…”

Section: Discussionmentioning

confidence: 99%

Nicotinamide mononucleotide attenuates glucocorticoid‑induced osteogenic inhibition by regulating the SIRT1/PGC‑1α signaling pathway

Huang

Tao

2020

Mol Med Rep

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long-term and high-dose glucocorticoid treatment is recognized as an important influencing factor for osteoporosis and osteonecrosis. nicotinamide mononucleotide (NMN) is an intermediate of NAD + biosynthesis, and is widely used to replenish the levels of NAD +. However, the potential role of NMN in glucocorticoid-induced osteogenic inhibition remains to be demonstrated. in the present study, the protective effects of NMN on dexamethasone (Dex)-induced osteogenic inhibition, and its underlying mechanisms, were investigated. Bone mesenchymal stem cells were treated with Dex, which decreased the levels of the osteogenic markers alkaline phosphatase, runt-related transcription factor 2 and osteocalcin. NMN treatment attenuated Dex-induced osteogenic inhibition and promoted the expression of sirtuin 1 (SIRT1) and peroxisome proliferator-activated receptor gamma coactivator (PGc)-1α. SirT1 knockdown reversed the protective effects of NMN and reduced the expression levels of PGC-1α. Collectively, the results of the present study reveal that nMn may be a potential therapeutic target for glucocorticoid-induced osteoporosis.

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Nicotinamide mononucleotide alleviates Aluminum induced bone loss by inhibiting the TXNIP-NLRP3 inflammasome

Cited by 31 publications

References 35 publications

Nicotinamide Mononucleotide: A Promising Molecule for Therapy of Diverse Diseases by Targeting NAD+ Metabolism

Nicotinamide Mononucleotide: A Promising Molecule for Therapy of Diverse Diseases by Targeting NAD+ Metabolism

The Role of NLRP3 Inflammasome Activities in Bone Diseases and Vascular Calcification

Nicotinamide mononucleotide attenuates glucocorticoid‑induced osteogenic inhibition by regulating the SIRT1/PGC‑1α signaling pathway

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