ArticleMolecular medicine reports2020
Hypoxia/reoxygenation activates the JNK pathway and accelerates synovial senescence.
Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Effectiveness of Different Telerehabilitation Strategies on Pain and Physical Function in Patients With Knee Osteoarthritis: Systematic Review and Meta-Analysis.Journal of medical Internet research · 2023Pooled it
- Research progress of mesenchymal stem cells/stromal cells and their derivatives against cell senescence in the treatment of osteoarthritis.Annals of medicine · 2026Review
- IGFBP5 alleviates periodontitis by reversing human dental follicle stem cell senescence via the non-canonical Wnt pathway.International journal of oral science · 2026Article
- Inflammaging and immunosenescence-driven remodeling of the immune microenvironment in osteoarthritis: mechanisms, immune regulation and immune reprogramming.Frontiers in immunology · 2026Review
- Synovial Fluid-derived Micrococcus Luteus G18 Exacerbates Osteoarthritis Progression by Promoting Chondrocyte Degradation via TLR2/JNK/AP-1 Signaling Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The drug discovery and therapeutic nano-strategies targeting cellular senescence.Materials today. Bio · 2025Review
- Targeting the senescence-associated secretory phenotype to modify osteoarthritis in aging.Inflammopharmacology · 2025Review
- Article
- The Role of Mitochondrial Permeability Transition in Bone Metabolism, Bone Healing, and Bone Diseases.Biomolecules · 2024Review
- Placental Tissue Calcification and Its Molecular Pathways in Female Patients with Late-Onset Preeclampsia.Biomolecules · 2024Article
- TIPE2 gene transfer ameliorates aging-associated osteoarthritis in a progeria mouse model by reducing inflammation and cellular senescence.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Endometrial senescence is mediated by interleukin 17 receptor B signaling.Cell communication and signaling : CCS · 2024Article
- Cadmium-induced annulus fibrosus cell senescence contributes to intervertebral disc degeneration via the JNK/p53 signaling pathway.Iranian journal of basic medical sciences · 2024Article
- Article
- c-Jun N-terminal kinase signaling in cellular senescence.Archives of toxicology · 2023Review
- Geniposide augments apoptosis in fibroblast-like synoviocytes by restoring hypoxia-enhanced JNK-BNIP3-mediated autophagy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Ceria Nanoparticles Alleviated Osteoarthritis through Attenuating Senescence and Senescence-Associated Secretory Phenotype in Synoviocytes.International journal of molecular sciences · 2023Article
- The molecular link between obstructive sleep apnea and osteoarthritis: based on bioinformatics analysis and experimental validation.American journal of translational research · 2023Article
- Soluble inflammatory mediators of synoviocytes stimulated by monosodium urate crystals induce the production of oxidative stress, pain, and inflammation mediators in chondrocytes : Secretome of synoviocytes induces chondrocyte damage.Clinical rheumatology · 2021Article
- Molecular mechanisms of mechanical load-induced osteoarthritis.International orthopaedics · 2021Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypoxia/reoxygenation (H/R) may play an important role via senescence in the mechanism of osteoarthritis (OA) development. The synovial membrane is highly sensitive to H/R due to its oxygen consumption feature. Excessive mechanical loads and oxidative stress caused by H/R induce a senescence‑associated secretory phenotype (SASP), which is related to the development of OA. The aim of the present study was to investigate the differences of SASP manifestation in synovial tissue masses between tissues from healthy controls and patients with OA. The present study used tumor necrosis factor‑α (TNF‑α) to pre‑treat synovial tissue and fibroblast‑like synoviocytes (FLS) to observe the effect of inflammatory cytokines on the synovial membrane before H/R. It was determined that H/R increased interleukin (IL)‑1β and IL‑6 expression levels in TNF‑α‑induced cell culture supernatants, increased the proportion of SA‑β‑gal staining, and increased the expression levels of high mobility group box 1, caspase‑8, p16, p21, matrix metalloproteinase (MMP)‑3 and MMP‑13 in the synovium. Furthermore, H/R opened the mitochondrial permeability transition pore, caused the loss of mitochondrial membrane potential (ΔΨm) and increased the release of reactive oxygen species (ROS). Moreover, H/R caused the expansion of the mitochondrial matrix and rupture of the mitochondrial extracorporeal membrane, with a decrease in the number of cristae. In addition, H/R induced activation of the JNK signaling pathway in FLS to induce cell senescence. Thus, the present results indicated that H/R may cause inflammation and escalate synovial inflammation induced by TNF‑α, which may lead to the pathogenesis of OA by increasing changes in synovial SASP and activating the JNK signaling pathway. Therefore, further studies expanding on the understanding of the pathogenesis of H/R etiology in OA are required.
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