ArticleAging cell2025
Senolytic therapy combining Dasatinib and Quercetin restores the chondrogenic phenotype of human osteoarthritic chondrocytes by the release of pro-anabolic mediators.
Article in Aging cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Immune dysregulation in osteoarthritis: Mechanisms, biomarkers, and therapeutic opportunities.Journal of translational autoimmunity · 2026Review
- Pathophysiology-guided biomarkers and therapeutics for precision trauma medicine in polytrauma with musculoskeletal injuries.Military Medical Research · 2026Review
- Orthogonal Light- and Enzyme-Triggered and-Gate Prodrugs for Senolytic Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Pharmacological targeting of the senescence-associated secretory phenotype in atherosclerosis: therapeutic potential of senolytics and senomorphics.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Comparative Phytochemical Profiling and Phenotypic Senolytic Screening of Botanical Extracts for Oxidative-Stress-Induced Skin-Cell Senescence.Antioxidants (Basel, Switzerland) · 2026Article
- Cellular senescence and aging: molecular mechanisms and convergent pathways.Cellular and molecular life sciences : CMLS · 2026Review
- Multi-omics profiling reveals systemic rejuvenation of the aged kidney through senolytic therapy.NPJ Regenerative medicine · 2026Article
- Protocol to quantify cell-surface vimentin on senescent human chondrocytes and other cell types via a cell-based ELISA.STAR protocols · 2026Article
- Exposure to high doses of tyre antioxidant 6PPD causes senescence to induce unexplained miscarriage by suppressing BAZ1B-mediated ubiquitination degradation of P21.EBioMedicine · 2026Article
- Cellular senescence as a therapeutic target for aging intervention.Biomedical journal · 2026Review
- Targeting Hyperoxia-Induced Cellular Senescence in Developing Human Airway Cells: Senomorphics Versus Senolytics Versus Antioxidants.Aging cell · 2026Article
- Exploring the Senotherapeutic Potential of Polyphenols in Aging and Disease: A Literature Review.International journal of molecular sciences · 2026Review
- Discovery of potent kinase inhibitors with improved pharmacokinetics and safety potentials through structural optimization of dasatinib.Communications medicine · 2026Article
- Senescence-associated gene pathways are differentially expressed in equine aging-related osteoarthritis.American journal of veterinary research · 2026Article
- Injectable microgels carrying engineered biomimetic nanoparticles for osteoarthritis therapy via dual-targeted senescent chondrocyte clearance and endogenous repair promotion.Bioactive materials · 2026Article
- Senolytic treatment induces oligodendrocyte dysfunction and demyelination in the corpus callosum.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Lactate-driven lactylation reprograms chondrocyte fate and joint inflammation in osteoarthritis: linking metabolism with epigenetic regulation.Frontiers in cell and developmental biology · 2026Review
- Recent Advances in Therapeutic Approaches for Knee Osteoarthritis: a Narrative Review.Biomolecules & therapeutics · 2026Review
- Senotherapeutics for Brain Aging Management.Neurology international · 2025Review
- Targeting the CXCL12/CXCR4 pathway by an optimized derivative or EPI-X4 preserves chondrocyte function and offers a novel therapeutic approach in rheumatic diseases.Arthritis research & therapy · 2025Article
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Abstract
Cellular senescence is associated with various age-related disorders and is assumed to play a major role in the pathogenesis of osteoarthritis (OA). Based on this, we tested a senolytic combination therapy using Dasatinib (D) and Quercetin (Q) on aged isolated human articular chondrocytes (hACs), as well as in OA-affected cartilage tissue (OARSI grade 1-2). Stimulation with D + Q selectively eliminated senescent cells in both, cartilage explants and isolated hAC. Furthermore, the therapy significantly promoted chondroanabolism, as demonstrated by increased gene expression levels of COL2A1, ACAN, and SOX9, as well as elevated collagen type II and glycosaminoglycan biosynthesis. Additionally, D + Q treatment significantly reduced the release of SASP factors (IL6, CXCL1). RNA sequencing analysis revealed an upregulation of the anabolic factors, inter alia, FGF18, IGF1, and TGFB2, as well as inhibitory effects on cytokines and the YAP-1 signaling pathway, explaining the underlying mechanism of the chondroanabolic promotion upon senolytic treatment. Accordingly, stimulation of untreated hAC with conditioned medium of D + Q-treated cells similarly induced the expression of chondrogenic markers. Detailed analyses demonstrated that chondroanabolic effects could be mainly attributed to Dasatinib, while monotherapeutical application of Quercetin or Navitoclax did not promote the chondroanabolism. Overall, D + Q therapy restored the chondrogenic phenotype in OA hAC most likely by creating a pro-chondroanabolic environment through the reduction of SASP factors and upregulation of growth factors. This senolytic approach could therefore be a promising candidate for further testing as a disease-modifying osteoarthritis drug.
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