ArticleFrontiers in immunology2023
Selenomethionine against titanium particle-induced osteolysis by regulating the ROS-dependent NLRP3 inflammasome activation via the β-catenin signaling pathway.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Biomimetic nanodelivery of antagomiR-155-5p ameliorates wear particle-induced osteolysis by dual regulation of Gas6/Axl-mediated macrophage inflammation.Journal of orthopaedic translation · 2026Article
- Implant-derived titanium particles impair macrophage bacterial clearance via TRPC1 and lysosomal dysfunction.PNAS nexus · 2026Article
- The protective effects of selenium against NLRP3-mediated inflammation and pyroptosis: mechanisms and the potential health benefits.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Review
- Repeated exposure to CoCr28Mo6 particles leads to activation of NLRP3 inflammasome signaling in human osteoblasts.Cell biology and toxicology · 2025Article
- Microbial Dysbiosis, Titanium Release, and Peri-implantitis.Journal of dental research · 2025Review
- Acid-responsive CST@NPs enhanced diabetic wound healing through rescuing mitochondrial dysfunction.Bioactive materials · 2025Article
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Authors and funding
17 authors.
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Abstract
Wear debris-induced osteolysis, especially titanium (Ti) particles-induced osteolysis, is the most common cause of arthroplasty failure with no effective therapy. Previous studies have suggested that inflammation and impaired osteogenesis are associated with Ti particles -induced osteolysis. Selenium (Se) is an essential trace element in the human body, which forms selenomethionine (Se-Met) in nature, and selenoproteins has strong anti-inflammatory and antioxidant stress effects. In this study, the effects of Se-Met on Ti particles-induced osteolysis were observed and the potential mechanism was explored. We found that exogenous Se-Met relieved osteolysis induced by Ti particles in two animal models and MC3T3-E1 cells. We found that the addition of Se-Met effectively inhibited Ti particle-induced inflammation by regulating reactive oxygen species-dependent (ROS-dependent) NOD-like receptor protein 3 (NLRP3) inflammasome activation. These therapeutic effects were abrogated in MC3T3-E1 cells that had received a β-catenin antagonist, suggesting that Se-Met alleviates inflammatory osteolysis via the β-catenin signaling pathway. Collectively, these findings indicated that Se-Met may serve as a potential therapeutic agent for treating Ti particle-induced osteolysis.
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