ArticleInternational journal of molecular medicine2021
Apremilast prevents IL‑17‑induced cellular senescence in ATDC5 chondrocytes mediated by SIRT1.
Article in International journal of molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- Phosphodiesterase inhibitors as emerging therapeutics for skeletal disorders: A comprehensive review of mechanisms and repurposing potential.Bone reports · 2026Review
- Chondrocyte Senescence in Osteoarthritis: Potential Targets and Pharmacological Interventions.Cartilage · 2026Article
- Single-Cell Transcriptomics Reveals Riluzole as an Osteoarthritis Candidate Drug via OB-NE Signaling Modulation and CTSS/NOS1 Inhibition.Drug design, development and therapy · 2026Article
- Evodiamine alleviates IL-1β-induced chondrocyte damage by regulating mitochondrial dysfunction via the SIRT1/PGC-1α pathway.Journal of molecular histology · 2025Article
- Aging: the wound that never starts healing.Nature communications · 2025Review
- Apremilast in osteoarthritis: exploring its therapeutic mechanisms.Drugs in context · 2025Review
- Osteoimmunology in Osteoarthritis: Unraveling the Interplay of Immunity, Inflammation, and Joint Degeneration.Journal of inflammation research · 2025Review
- New insights into the role of cellular senescence and rheumatic diseases.Frontiers in immunology · 2025Review
- Therapeutic role of aripiprazole in cartilage defects explored through a drug repurposing approach.Scientific reports · 2024Article
- A signaling pathway map of plasminogen activator inhibitor-1 (PAI-1/SERPINE-1): a review of an innovative frontier in molecular aging and cellular senescence.Cell communication and signaling : CCS · 2024Review
- Roflumilast Attenuates Microglial Senescence and Retinal Inflammatory Neurodegeneration Post Retinal Ischemia Reperfusion Injury Through Inhibiting NLRP3 Inflammasome.Investigative ophthalmology & visual science · 2024Article
- S100A4 targets PPP1CA/IL-17 to inhibit the senescence of sheep endometrial epithelial cells.Frontiers in veterinary science · 2024Article
- Article
- IL-17 in osteoarthritis: A narrative review.Open life sciences · 2023Review
- Sirtuins in osteoarthritis: current understanding.Frontiers in immunology · 2023Review
- Aging and aging-related diseases: from molecular mechanisms to interventions and treatments.Signal transduction and targeted therapy · 2022Review
- Development of Apremilast Nanoemulsion-Loaded Chitosan Gels: In Vitro Evaluations and Anti-Inflammatory and Wound Healing Studies on a Rat Model.Gels (Basel, Switzerland) · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis is the most prevalent joint degenerative disease and has been considered a major cause of severe joint pain and physical disability in the elderly. The chondrocyte is the only cell type found in articular cartilage and chondrocyte senescence plays a pivotal role in the pathogenesis of osteoarthritis. Apremilast is an oral PDE4 inhibitor and has been used for the treatment of patients with active psoriatic arthritis. In the present study, the biological function of apremilast was examined in an interleukin (IL)‑17‑treated chondrocyte model. Expression levels of target genes and proteins were measured using reverse transcription‑quantitative PCR, ELISA, and western blotting, respectively. ROS levels in chondrocytes were examined using the fluorescent dye DCFH‑DA. Cellular senescence was determined using senescence-associated-β-galactosidase staining. The profile of cell cycle phases was analyzed via flow cytometry. It was revealed that treatment with apremilast reduced the expression of IL‑1β, MCP‑1, and the production of ROS. SA‑β‑gal staining results indicated that the presence of apremilast suppressed IL‑17‑induced cellular senescence. Furthermore, apremilast prevented IL‑17‑induced G0/G1 phase cell cycle arrest. In addition, it was demonstrated that apremilast suppressed IL‑17‑induced expression of p21 and PAI‑1. Notably, the silencing of sirtuin 1 (SIRT1) abolished the protective effect of apremilast against IL‑17‑induced cellular senescence, suggesting that the action of apremilast in chondrocytes is dependent on SIRT1. In conclusion, the present results revealed that apremilast exerted a beneficial effect, thereby protecting chondrocytes from senescence induced by IL‑17.
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