ArticleStem cell research & therapy2025
Senescent bone marrow mesenchymal stem cells exacerbate subchondral bone sclerosis and osteoarthritis via the senescence-associated secretory phenotype.
Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- From pathogenic to reparative: Context-Dependent function of extracellular vesicles in osteoarthritis.Bioactive materials · 2027Review
- Stem cell senescence as a regenerative bottleneck in age-related skeletal degeneration: Mechanistic crosstalk and translational strategies.Regenerative therapy · 2026Review
- Mechanistic Links Underlying the Comorbidity of Osteoporosis and Osteoarthritis: Cell Fate Plasticity Driven by the Subchondral Bone Microenvironment.International journal of molecular sciences · 2026Review
- The multilayer coatings on polylactic acid implants spatiotemporally regulates the microenvironment to enhance antibacterial and osseointegration capacity.Materials today. Bio · 2026Article
- HIF-1α-centered metabolic reprogramming in osteoarthritis: cell type-specific effects and intercellular crosstalk among chondrocytes, BMSCs, and macrophages.Frontiers in immunology · 2026Review
- Aging-related metabolic dysregulation in osteoporosis: mechanisms and therapeutic strategies.Frontiers in aging · 2026Review
- Identification and validation of SUMOylation-related key genes for osteoarthritis through integration of single-cell, bulk RNA sequencing and animal model experiments.Frontiers in medicine · 2026Article
- Senescence-associated secretory phenotype: the "pathogenic" factor driving orthopedic degenerative diseases and its regulation.Frontiers in aging · 2026Review
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10 authors.
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Abstract
backgroundOsteoarthritis (OA) is a common joint disease characterized by articular cartilage degeneration, with subchondral bone sclerosis being a key pathological change. However, the mechanism underlying subchondral bone sclerosis remains unclear. Senescent stem cells have been found in OA cartilage, synovium, and subchondral bone. This study aimed to explore the role of senescent bone marrow mesenchymal stem cells (BMSCs) in subchondral bone sclerosis and OA progression.
methodsThis study utilized two mouse OA models: closed anterior cruciate ligament transection and spontaneous OA. Immunostaining was performed to assess the proportion of senescent cells especially BMSCs in subchondral bone during OA progression. A senescence model of BMSCs was constructed using H₂O₂, and transcriptomic sequencing was conducted to analyze secretory phenotypic changes in senescent BMSCs. In vitro experiments were performed to evaluate the effects of senescent BMSC-derived senescence-associated secretory phenotype (SASP) on osteogenic differentiation and osteogenic marker expression in normal BMSCs. We examined the mRNA expression of core molecules in osteogenesis-related pathways, which were activated by SASP. Additionally, OA mice were administered the senolytic combination of dasatinib and quercetin (D + Q), and its effects on senescent BMSCs, osteocalcin expression, subchondral bone sclerosis, and OA progression were assessed.
resultsImmunostaining results showed a significant increase in the proportion of senescent BMSCs in subchondral bone during OA progression. Transcriptomic sequencing revealed that senescent BMSCs acquired the SASP. In vitro experiments demonstrated that conditioned medium from senescent BMSCs (containing SASP) significantly promoted osteogenic differentiation and upregulated the expression of osteogenic markers in normal BMSCs. The SASP significantly upregulated Mapk8 and Mapk14 mRNAs in osteogenesis-related pathways. Administration of D + Q to OA mice effectively cleared senescent BMSCs, reduced osteocalcin expression in subchondral bone, inhibited subchondral bone sclerosis, and alleviated OA progression.
conclusionsThis study indicates that senescent BMSCs promote subchondral bone sclerosis and OA progression through activating Mapk8 and Mapk14 via SASP in subchondral bone. The senolytic combination D + Q holds potential for OA treatment by eliminating senescent BMSCs in subchondral bone.
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