ArticleCell death discovery2022
MiR-92a/KLF4/p110δ regulates titanium particles-induced macrophages inflammation and osteolysis.
Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 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
- TRIM30a coordinates neutrophil-macrophage crosstalk to resolve inflammation and drive osseointegration via suppressing NETosis/cGAS-STING axis.Materials today. Bio · 2026Article
- MiR-7a-Klf4 axis as a regulator and therapeutic target of neuroinflammation and ferroptosis in Alzheimer's disease.NAR molecular medicine · 2025Article
- The dual role of titanium particles in osteolysis: implications for gene therapy in prosthesis loosening.European journal of medical research · 2025Article
- Case Report: Prosthetic revision due to aseptic loosening following total knee arthroplasty: a clinical management and pathological mechanism investigation.Frontiers in surgery · 2025Article
- Expression of miR-92a in Green Tea EGCG Preconditioned Adiposederived Stem Cells Ameliorates Inflammatory Response and Increases Cartilage Regeneration in RA Rats through KLF4/IL-17/MMP-2 Axis Modulation.Current gene therapy · 2025Article
- Efferocytosis-induced metabolic shift in bone macrophages drives lactate production and modulates inflammation and osteoclastogenesis.Frontiers in immunology · 2025Article
- Identification of potential key circular RNAs associated with Escherichia coli-infected bovine mastitis using RNA-sequencing: preliminary study results.Veterinary research communications · 2024Article
- Byakangelicol suppresses TiPs-stimulated osteoclastogenesis and bone destruction via COX-2/NF-κB signaling pathway.Regenerative biomaterials · 2024Article
- MicroRNAs in Aseptic Loosening of Prosthesis: Pathophysiology and Potential Therapeutic Approaches.The archives of bone and joint surgery · 2024Review
- Titanium particles in peri-implantitis: distribution, pathogenesis and prospects.International journal of oral science · 2023Review
- Inhibition of miR-25 Ameliorates Cardiac Dysfunction and Fibrosis by Restoring Krüppel-like Factor 4 Expression.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
As total joint replacement is widely applied for severe arthropathy, peri-prosthetic aseptic loosening as one of the main causes of implant failure has drawn wide attention. Wear particles such as titanium particles (TiPs) derived from prosthesis can initiate macrophages inflammation and sequentially activate osteoclasts, which results in bone resorption and osteolysis for long-term. Therefore, inhibiting wear particles induced macrophages inflammation is considered as a promising therapy for AL. In this research, we found that the inhibition of p110δ, a member of class IA PI3Ks family, could significantly dampen the TiPs-induced secretion of TNFα and IL-6. By the transfection of siRNA targeting p110δ, we confirmed that p110δ was responsible for TNFα and IL-6 trafficking out of Golgi complex without affecting their expression in TiPs-treated macrophages. As the upstream transcription-repressor of p110δ, Krüppel-like factor 4 (KLF4), targeted by miR-92a, could also attenuate TiPs-induced inflammation by mediating NF-κB pathway and M1/M2 polarization. To further ascertain the roles of KLF4/p110δ, TiPs-induced mice cranial osteolysis model was established and vivo experiments validated that KLF4-knockdown could exacerbate TiPs-induced osteolysis, which was strikingly ameliorated by knockdown of p110δ. In summary, our study suggests the key role of miR-92a/KLF4/p110δ signal in TiPs-induced macrophages inflammation and osteolysis.
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Registered trials
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