ArticleNature communications2022
Inhibitory role of Annexin A1 in pathological bone resorption and therapeutic implications in periprosthetic osteolysis.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
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- Identifying Myeloid-Derived Suppressor Cells and Lipocalin-2 as Therapeutic Targets for Intervertebral Disc Degeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Fused exosomal targeted therapy in periprosthetic osteolysis through regulation of bone metabolic homeostasis.Bioactive materials · 2025Article
- PPARγ controls ESCRT-dependent fibroblast-like synoviocyte exosome biogenesis and alleviates chondrocyte osteoarthritis mediated by exosomal ANXA1.Journal of orthopaedic translation · 2025Article
- Evaluation of annexin A1, carbonic anhydrase 1, and elongation factor 1-gamma levels in periodontal diseases.BMC oral health · 2025Article
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- Single-cell multi-omics identify novel regulators required for osteoclastogenesis during aging.iScience · 2024Article
- Preventing periprosthetic osteolysis in aging populations through lymphatic activation and stem cell-associated secretory phenotype inhibition.Communications biology · 2024Article
- In Vitro Insights into the Role of 7,8-Epoxy-11-Sinulariolide Acetate Isolated from Soft CoralMarine drugs · 2024Article
- Development of Ac2-26 Mesoporous Microparticle System as a Potential Therapeutic Agent for Inflammatory Bowel Diseases.International journal of nanomedicine · 2024Article
- Periapical lesion-derived decellularized extracellular matrix as a potential solution for regenerative endodontics.Regenerative biomaterials · 2024Article
- Extracellular vesicles derived from dental follicle stem cells regulate tooth eruption by inhibiting osteoclast differentiation.Frontiers in cell and developmental biology · 2024Article
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Authors and funding
15 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is currently no therapy available for periprosthetic osteolysis, the most common cause of arthroplasty failure. Here, the role of AnxA1 in periprosthetic osteolysis and potential therapeutics were investigated. Reducing the expression of AnxA1 in calvarial tissue was found to be associated with increased osteolytic lesions and the osteolytic lesions induced by debris implantation were more severe in AnxA1-defecient mice than in wild-type mice. AnxA1 inhibits the differentiation of osteoclasts through suppressing NFκB signaling and promoting the PPAR-γ pathway. Administration of N-terminal-AnxA1 (Ac2-26 peptide) onto calvariae significantly reduced osteolytic lesions triggered by wear debris. These therapeutic effects were abrogated in mice that had received the PPAR-γ antagonist, suggesting that the AnxA1/PPAR-γ axis has an inhibitory role in osteolysis. The administration of Ac2-26 suppressed osteolysis induced by TNF-α and RANKL injections in mice. These findings indicate that AnxA1 is a potential therapeutic agent for the treatment of periprosthetic osteolysis.
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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.