ArticleArthritis & rheumatology (Hoboken, N.J.)2023
Association of Dipeptidylpeptidase 4 (CD26) With Chondrocyte Senescence and Radiographic Progression in Knee Osteoarthritis.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 27 citations in OpenAlex.
- A compendium of circulating biomarkers of senescence in humans: Insights on mechanistic impact across health domains and modulation by therapeutic interventions.Ageing research reviews · 2026Review
- Hydrogels as Local Structural-Protective Platforms in Rheumatoid Arthritis: An Evidence-Graded Review Across the Synovium-Cartilage-Bone Axis.Gels (Basel, Switzerland) · 2026Review
- Synergistic targeting of senolytic and senomorphic action with dual-engineered biomimetic macrophage nanovesicles for mitigating osteoarthritis.Bioactive materials · 2026Article
- The ganglioside GD3 and its synthase (ST8SIA1) as novel senescence markers associated with osteoarthritis.GeroScience · 2026Article
- Chimeric Antigen Receptor T Cells as Living Therapeutics Targeting Senescence and Age-Related Diseases.Research (Washington, D.C.) · 2026Review
- Paradigm shift in macrophage polarization in osteoarthritis: from M1/M2 imbalance to macrophage state reprogramming in the ageing immune microenvironment.Frontiers in immunology · 2026Review
- The osteoarthritis inflammatory ecosystem: a node-edge-boundary-emergent framework toward precision stratification and therapeutic hypothesis generation.Frontiers in medicine · 2026Review
- Dipeptidyl peptidase-4 inhibitors are associated with a lower risk of osteoarthritis in patients with type 2 diabetes.Therapeutic advances in musculoskeletal disease · 2026Article
- Review
- Towards stratification in osteoarthritis: a review of the scientific terminology used in published basic research.BMC rheumatology · 2025Review
- Chimeric Antigen Receptor Cell Therapy: Current Status and Its Potential in Aging and Alzheimer's Disease.International journal of molecular sciences · 2025Review
- RO5126766 attenuates osteoarthritis by inhibiting osteoclastogenesis and protecting chondrocytes through mediating the ERK pathway.Journal of orthopaedic translation · 2025Article
- Dipeptidyl Peptidase 4 (DPP4) Exacerbates Osteoarthritis Progression in an Enzyme-Independent Manner.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- GATD3A-deficiency-induced mitochondrial dysfunction facilitates senescence of fibroblast-like synoviocytes and osteoarthritis progression.Nature communications · 2024Article
- Targeting FAP-positive chondrocytes in osteoarthritis: a novel lipid nanoparticle siRNA approach to mitigate cartilage degeneration.Journal of nanobiotechnology · 2024Article
- Selective targeting of dipeptidyl-peptidase 4 (DPP-4) positive senescent chondrocyte ameliorates osteoarthritis progression.Aging cell · 2024Article
- A Novel Role for Protein Tyrosine Phosphatase 1B in Alleviating Chondrocyte Senescence.ACS omega · 2024Article
- Aging and the emerging role of cellular senescence in osteoarthritis.Osteoarthritis and cartilage · 2024Review
- Research progress of procyanidins in repairing cartilage injury after anterior cruciate ligament tear.Heliyon · 2024Review
- Proteomic profiling of human menisci from mild joint degeneration and end-stage osteoarthritis versus healthy controls.Osteoarthritis and cartilage open · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
objectiveTo evaluate the association of dipeptidylpeptidase 4 (DPP-4; also known as CD26) with cellular senescence of human cartilage and progression of knee osteoarthritis (OA).
methodsArticular cartilage sections and chondrocytes were acquired from 35 individuals undergoing total knee replacement for OA to evaluate the following: 1) the association between OA severity and established senescence markers (senescence-associated β-galactosidase activity and p16), which was quantified using immunohistochemistry and flow cytometry (n = 19 samples); 2) the coexpression of DPP-4 with established senescence markers, which was assessed using flow cytometry; and 3) expression levels of anabolic and catabolic genes, senescence-related genes, and senescence-associated secretory phenotypes in DPP-4+ and DPP-4- cells, which were isolated using fluorescence-activated cell sorting or magnetic-activated cell sorting (n = 16 samples). The concentration of soluble DPP-4 was measured in samples of synovial fluid and samples of plasma from the Prediction of Osteoarthritis Progression cohort and then evaluated for association with the severity of radiographic knee OA at baseline (n = 65 samples) and the progression of structural radiographic OA (n = 57 samples) over a 3-year period.
resultsDPP-4 expression was associated with higher senescence-associated β-galactosidase activity, p16 expression, senescence-related gene and catabolic gene (ADAMTS5, MMP13, IL6, and IL8) expression, higher senescence-associated secretory phenotype secretion, and lower anabolic gene (COL2A1 and ACAN) expression in primary chondrocytes. Synovial fluid DPP-4 concentration was associated with radiographic OA progression (odds ratio 105.32; P = 0.015), proteases (synovial fluid matrix metalloproteinase 1 and matrix metalloproteinase 3), aggrecan degradation (synovial fluid sulfated glycosaminoglycan), indicators of activated macrophages (synovial fluid CD14 and CD163), and inflammation (synovial fluid interleukin-6).
conclusionOur study identifies DPP-4 as a key surface marker in senescent chondrocytes and a predictor of radiographic OA progression.
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