ArticleCell proliferation2021
CoCrMo-Nanoparticles induced peri-implant osteolysis by promoting osteoblast ferroptosis via regulating Nrf2-ARE signalling pathway.
Article in Cell proliferation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 46 citations in OpenAlex.
- Ferroptosis in compromised bone healing after trauma: from the iron/ROS microenvironment to non-union and bone defect reconstruction.Frontiers in medicine · 2026Review
- Ferroptosis in orthopedic implant integration after oncologic surgery.Frontiers in oncology · 2026Review
- YTHDF1 transcriptionally activated by TCF4 suppresses osteoblast ferroptosis in titanium nanoparticle-induced osteolysis by accelerating GPX4 and SLC7A11 translation.Journal of nanobiotechnology · 2025Article
- Ferroptosis Inhibition Enhances Osteoblast Activity: The Role of Liproxstatin-1 and Coenzyme Q10.International journal of molecular sciences · 2025Article
- Repeated exposure to CoCr28Mo6 particles leads to activation of NLRP3 inflammasome signaling in human osteoblasts.Cell biology and toxicology · 2025Article
- The Role of Nrf2 in the Regulation of Periodontitis, Peri-implantitis, Dentin Infection, and Apical Periodontitis.Biological procedures online · 2025Review
- Application of integrated omics in aseptic loosening of prostheses after hip replacement.Molecular medicine reports · 2025Article
- Article
- Ferrostatin-1 inhibits osteoclast differentiation and prevents osteoporosis by suppressing lipid peroxidation.Journal of orthopaedic surgery and research · 2025Article
- Therapeutic Potential of Targeting Ferroptosis in Periprosthetic Osteolysis Induced by Ultra-High-Molecular-Weight Polyethylene Wear Debris.Biomedicines · 2025Article
- Osteoblastic ferroptosis inhibition by small-molecule promoting GPX4 activation for peri-prosthetic osteolysis therapy.Journal of nanobiotechnology · 2024Article
- DNMT aberration-incurred GPX4 suppression prompts osteoblast ferroptosis and osteoporosis.Bone research · 2024Article
- The Role and Interactive Mechanism of Endoplasmic Reticulum Stress and Ferroptosis in Musculoskeletal Disorders.Biomolecules · 2024Review
- Repair and regeneration: ferroptosis in the process of remodeling and fibrosis in impaired organs.Cell death discovery · 2024Review
- DNA Methylation-Mediated GPX4 Transcriptional Repression and Osteoblast Ferroptosis Promote Titanium Particle-Induced Osteolysis.Research (Washington, D.C.) · 2024Article
- Influence of metallic particles and TNF on the transcriptional regulation of NLRP3 inflammasome-associated genes in human osteoblasts.Frontiers in immunology · 2024Article
- Ferroptosis in pancreatic diseases: potential opportunities and challenges that require attention.Human cell · 2023Review
- SOST gene suppression stimulates osteocyte Wnt/β-catenin signaling to prevent bone resorption and attenuates particle-induced osteolysis.Journal of molecular medicine (Berlin, Germany) · 2023Article
- The dual role of autophagy in periprosthetic osteolysis.Frontiers in cell and developmental biology · 2023Review
- ALDH3B1 protects interfollicular epidermal cells against lipid peroxidation via the NRF2 pathway.Cell stress & chaperones · 2022Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
objectivesAseptic loosening (AL) is the most common reason of total hip arthroplasty (THA) failure and revision surgery. Osteolysis, caused by wear particles released from implant surfaces, has a vital role in AL. Although previous studies suggest that wear particles always lead to osteoblast programmed death in the process of AL, the specific mechanism remains incompletely understood and osteoblast ferroptosis maybe a new mechanism of AL. MATERIALS AND
methodsCoCrMo nanoparticles (CoNPs) were prepared to investigate the influence of ferroptosis in osteoblasts and calvaria resorption animal models. Periprosthetic osteolytic bone tissue was collected from patients who underwent AL after THA to verify osteoblast ferroptosis.
resultsOur study demonstrated that CoNPs induced significant ferroptosis in osteoblasts and particles induced osteolysis (PIO) animal models. Blocking ferroptosis with specific inhibitor Ferrostatin-1 dramatically reduced particle-induced ferroptosis in vitro. Moreover, in osteoblasts, CoNPs significantly downregulated the expression of Nrf2 (nuclear factor erythroid 2-related factor 2), a core element in the antioxidant response. The overexpression of Nrf2 by siKeap1 or Nrf2 activator Oltipraz obviously upregulated antioxidant response elements (AREs) and suppressed ferroptosis in osteoblasts. Furthermore, in PIO animal models, the combined utilization of Ferrostatin-1 and Oltipraz dramatically ameliorated ferroptosis and the severity of osteolysis.
conclusionsThese results indicate that CoNPs promote osteoblast ferroptosis by regulating the Nrf2-ARE signalling pathway, which suggests a new mechanism underlying PIO and represents a potential therapeutic approach for AL.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.