Protective effects of sirtuin 3 on titanium particle-induced osteogenic inhibition by regulating the NLRP3 inflammasome via the GSK-3β/β-catenin signalling pathway

Zheng, Kai; Bai, Jiaxiang; Li, Ning; Li, Meng; Sun, Houyi; Zhang, Weicheng; Ge, Gaoran; Liang, Xiaoyao; Tao, Huaqiang; Xue, Yi; Hao, Yuefeng; Xu, Yaozeng; Geng, Dechun

doi:10.1016/j.bioactmat.2021.02.039

Cited by 25 publications

(28 citation statements)

References 46 publications

(34 reference statements)

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“…However, for the activation of NLRP3 and AIM2, SIRT3 is not necessary [ 112 ]. However, in a study conducted by K Zheng et al [ 113 ] on Ti-induced osteolysis of rat femurs, it was found that depletion of SIRT3 enhanced the activation of the NLRP3. The researchers also confirmed that the expression of SIRT3 in the revision TJA was significantly lower than that in the primary TJA through the investigation of clinical samples.…”

Section: Pyroptosis In Osteoblastmentioning

confidence: 99%

Pyroptosis in Periprosthetic Osteolysis

Yin

Peng

et al. 2022

Biomolecules

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Periprosthetic osteolysis (PPO) along with aseptic loosening (AL) caused by wear particles after artificial joint replacement is the key factor in surgical failure and subsequent revision surgery, however, the precise molecular mechanism underlying PPO remains unclear. Aseptic inflammation triggered by metal particles, resulting in the imbalance between bone formation by osteoblasts and bone resorption by osteoclasts may be the decisive factor. Pyroptosis is a new pro-inflammatory pattern of regulated cell death (RCD), mainly mediated by gasdermins (GSDMs) family, among which GSDMD is the best characterized. Recent evidence indicates that activation of NLRP3 inflammasomes and pyroptosis play a pivotal role in the pathological process of PPO. Here, we review the pathological process of PPO, the molecular mechanism of pyroptosis and the interventions to inhibit the inflammation and pyroptosis of different cells during the PPO. Conclusively, this review provides theoretical support for the search for new strategies and new targets for the treatment of PPO by inhibiting pyroptosis and inflammation.

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Section: Pyroptosis In Osteoblastmentioning

confidence: 99%

Pyroptosis in Periprosthetic Osteolysis

Yin

Peng

et al. 2022

Biomolecules

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“…Therefore, the SIRT3 and SOD2 may form an important regulatory network to protect osteoblasts against the cytotoxic of TiO2NPs ( 94 ). Besides, upregulation of SIRT3 significantly attenuates the titanium particle-induced inhibition of osteogenesis by inhibiting the NLRP3 inflammasome ( 95 ). To sum up, SIRT3 plays a protective role in bone formation and maintaining bone homeostasis.…”

Section: The Role Of Sirt3 In Bone Remodeling and Osteoporosismentioning

confidence: 99%

The Role of SIRT3 in the Osteoporosis

Wang

2022

Front. Endocrinol.

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SIRT3 is an NAD+-dependent deacetylase in the mitochondria with an extensive ability to regulate mitochondrial morphology and function. It has been reported that SIRT3 participates in the occurrence and development of many aging-related diseases. Osteoporosis is a common aging-related disease characterized by decreased bone mass and fragility fractures, which has caused a huge burden on society. Current research shows that SIRT3 is involved in the physiological processes of senescence of bone marrow mesenchymal stem cells (BMSCs), differentiation of BMSCs and osteoclasts. However, the specific effects and mechanisms of SIRT3 in osteoporosis are not clear. In the current review, we elaborated on the physiological functions of SIRT3, the cell types involved in bone remodeling, and the role of SIRT3 in osteoporosis. Furthermore, it also provided a theoretical basis for SIRT3 as a therapeutic target for osteoporosis.

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“…In contrast, the inhibitor of the TGF-β/Smad2/3 pathway did not affect the activation of ERK1/2, indicating that the activation effect of the ERK1/2 pathway triggered by TGF-β2 on regulating EMT was not controlled by the TGF-β/Smad pathway. Glycogen synthase kinase-3β (GSK-3β), a serine/threonine kinase widely found in mammalian cells, is closely related to cell proliferation, apoptosis, migration, and EMT [ [21] , [22] , [23] ] and can phosphorylate, ubiquitinate, or degrade transcription factors, including Snail and Slug to maintain epithelial phenotypes [ 24 , 25 ]. Therefore, we infer that when GSK-3β is phosphorylated and inactivated, the degradation of a range of downstream transcription factors, such as Snail and Slug, is limited, which can promote the development of EMT.…”

Section: Introductionmentioning

confidence: 99%

Drug-eluting intraocular lens with sustained bromfenac release for conquering posterior capsular opacification

Zhang

Lai

et al. 2022

Bioactive Materials

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Cataract is the leading cause of visual impairment, and posterior capsular opacification (PCO) is the most common long-term complication of modern cataract surgery, which can cause severe visual impairment after surgery. The proliferation, migration, and epithelial-mesenchymal transition (EMT) of residual lens epithelial cells (LECs) stimulated by growth factors and cytokines, are the key pathological mechanisms involved in the development of PCO. This study demonstrated that non-steroidal anti-inflammatory drug (NSAID), bromfenac, was capable of effectively inhibiting cell migration, overexpression of EMT markers, such as fibronectin (FN), matrix metalloproteinase 2 (MMP2), α-smooth muscle actin (α-SMA), and transcription factor Snail, and extracellular signal-regulated kinase (ERK)/glycogen synthase kinase-3β (GSK-3β) signaling induced by transforming growth factor-β2 (TGF-β2) in vitro . The inhibitory effect of bromfenac on TGF-β2-induced EMT was also verified on a primary lens epithelial cell model using human anterior capsules. Furthermore, based on ultrasonic spray technology, we developed a drug-eluting intraocular lens (IOL) using poly (lactic-co-glycolic acid) (PLGA) with sustained bromfenac release ability for the prevention of PCO development. In the rabbit models of cataract surgery, bromfenac-eluting IOL exhibited remarkable PCO prevention and inflammation suppression effects with excellent biocompatibility. In conclusion, bromfenac can inhibit TGF-β2-induced cell migration and the EMT of LECs via ERK/GSK-3β/Snail signaling. The present study offers a novel approach for preventing PCO through PLGA-based drug sustained-release IOLs.

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Protective effects of sirtuin 3 on titanium particle-induced osteogenic inhibition by regulating the NLRP3 inflammasome via the GSK-3β/β-catenin signalling pathway

Cited by 25 publications

References 46 publications

Pyroptosis in Periprosthetic Osteolysis

Pyroptosis in Periprosthetic Osteolysis

The Role of SIRT3 in the Osteoporosis

Drug-eluting intraocular lens with sustained bromfenac release for conquering posterior capsular opacification

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