ArticleAging2022
Increased expression of osteopontin in subchondral bone promotes bone turnover and remodeling, and accelerates the progression of OA in a mouse model.
Article in Aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Association between the prevalence of pulp stones and calcified atherosclerotic plaques: a systematic review and meta-analysis.Dento maxillo facial radiology · 2023Pooled it
- The emerging role of subchondral bone homeostasis in osteoarthritis.Journal of orthopaedic translation · 2026Review
- Review
- FSCN1 induces subchondral bone sclerosis in osteoarthritis via modulating actin cytoskeleton dynamics and YAP signaling.Arthritis research & therapy · 2026Article
- Network Pharmacology and Experimental Evidence Indicate That Dihydrochelerythrine fromJournal of inflammation research · 2026Article
- Adipose tissue inflammation mediated by CCL19 overexpression exacerbates experimental periodontitis via elevated circulating saturated fatty acids and osteopontin in Western-diet-fed mice.Frontiers in immunology · 2026Article
- Greening Bone Healing: The Emerging Role of Plant-Derived Exosome-Like Nanoparticles in Osteoporosis and Osteoarthritis Therapy.International journal of nanomedicine · 2026Review
- The crucial role of SPP1 in osteoporosis, osteoarthritis, and cancer.Pharmaceutical science advances · 2025Review
- Musculoskeletal Complications in COVID-19: Exploring the Role of Key Biomarkers.International journal of molecular sciences · 2025Review
- Exploring molecular disparities of H-type vasculature endothelial cells in osteonecrosis of the femoral head through single-cell analysis.BMC musculoskeletal disorders · 2025Article
- Denosumab ameliorates osteoarthritis by protecting cartilage against degradation and modulating subchondral bone remodeling.Regenerative therapy · 2024Article
- Osteopontin deficiency promotes cartilaginous endplate degeneration by enhancing the NF-κB signaling to recruit macrophages and activate the NLRP3 inflammasome.Bone research · 2024Article
- Signalling interaction between β-catenin and other signalling molecules during osteoarthritis development.Cell proliferation · 2024Review
- Pathological progression of osteoarthritis: a perspective on subchondral bone.Frontiers of medicine · 2024Review
- Targeting type H vessels in bone-related diseases.Journal of cellular and molecular medicine · 2024Review
- Osteopontin: A Bone-Derived Protein Involved in Rheumatoid Arthritis and Osteoarthritis Immunopathology.Biomolecules · 2023Review
- Single-cell RNA sequencing analysis of human chondrocytes reveals cell-cell communication alterations mediated by interactive signaling pathways in osteoarthritis.Frontiers in cell and developmental biology · 2023Article
- Mitochondrial Calcium Nanoregulators Reverse the Macrophage Proinflammatory Phenotype Through Restoring Mitochondrial Calcium Homeostasis for the Treatment of Osteoarthritis.International journal of nanomedicine · 2023Article
- Roles of circular RNAs in osteogenic differentiation of bone marrow mesenchymal stem cells (Review).Molecular medicine reports · 2022Review
- Osteopontin, a bridge links osteoarthritis and osteoporosis.Frontiers in endocrinology · 2022Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteopontin (OPN) has been proved to be closely related to the pathogenesis of osteoarthritis (OA), but the role of OPN in the pathogenesis of OA has not been fully clarified. Current studies on OPN in OA mostly focus on articular cartilage, synovial membrane and articular fluid, while ignoring its role in OA subchondral bone turnover and remodeling. In this study, we used a destabilization OA mouse model to investigate the role of OPN in OA subchondral bone changes. Our results indicate that increased expression of OPN accelerates the turnover and remodeling of OA subchondral bone, promotes the formation of h-type vessels in subchondral bone, and mediates articular cartilage degeneration induced by subchondral bone metabolism. In addition, our results confirmed that inhibition of PI3K/AKT signaling pathway inhibits OPN-mediated OA subchondral bone remodeling and cartilage degeneration. This study revealed the role and mechanism of OPN in OA subchondral bone, which is of great significance for exploring specific biological indicators for early diagnosis of OA and monitoring disease progression, as well as for developing drugs to regulate the metabolism and turnover of subchondral bone and alleviate the subchondral bone sclerosis of OA.
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Registered trials
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.