ArticleDrug design, development and therapy2019
Activation of the P38/CREB/MMP13 axis is associated with osteoarthritis.
Article in Drug design, development and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- CK2.1 Activates Chondrogenesis by Regulation of the p38 Mitogen-Activated Protein Kinase Pathway.Kinases and phosphatases · 2026Article
- Assessment of morphology, radiopacity gradient and mechanical properties of articular cartilage with contrast-enhanced high-resolution peripheral quantitative computed tomography.Frontiers in bioengineering and biotechnology · 2026Article
- Disruption of Morrbid alleviates autoinflammatory osteomyelitis in Pstpip2-deficient mice.Disease models & mechanisms · 2025Article
- Regulation of matrix metalloproteinase-13 in cancer: Signaling pathways and non-coding RNAs in tumor progression and therapeutic targeting.World journal of clinical oncology · 2025Review
- Comparison of passive and active motion: effect of myokine irisin on cartilage in knee osteoarthritis rats.Frontiers in physiology · 2025Article
- Bidirectional effects of morphine on pancreatic cancer progression via the p38/JNK pathway.Scientific reports · 2024Article
- Clinical Outcome of Multiple Platelet-Rich Plasma Injection and Correlation with PDGF-BB in the Treatment of Knee Osteoarthritis.Journal of personalized medicine · 2024Article
- Blocking IL-33 decelerates cartilage degeneration in knee osteoarthritis through mice model.PloS one · 2024Article
- HU308 Mitigates Osteoarthritis by Stimulating Sox9-Related Networks of Carbohydrate Metabolism.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023Article
- Glycolysis: an emerging regulator of osteoarthritis.Frontiers in immunology · 2023Review
- LncRNA SNHG5 Suppresses Cell Migration and Invasion of Human Lung Adenocarcinoma via Regulation of Epithelial-Mesenchymal Transition.Journal of oncology · 2023Article
- LTBP1 Gene Expression in the Cerebral Cortex and its Neuroprotective Mechanism in Mice with Postischemic Stroke Epilepsy.Current pharmaceutical biotechnology · 2023Article
- One session of 20 N cyclic compression induces chronic knee osteoarthritis in rats: A long-term study.Osteoarthritis and cartilage open · 2022Article
- The Metabolic Landscape in Osteoarthritis.Aging and disease · 2022Article
- Chaenomeles Fructus (CF), the Fruit ofInternational journal of molecular sciences · 2022Article
- MiR-19b-3p Attenuates Chondrocytes Injury by Inhibiting MAPK/NF-Κb Axis via Targeting SOCS1.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Recombinant platelet-derived growth factor-BB alleviates osteoarthritis in a rat model by decreasing chondrocyte apoptosis in vitro and in vivo.Journal of cellular and molecular medicine · 2021Article
- lncRNA SNHG16 promotes the occurrence of osteoarthritis by sponging miR‑373‑3p.Molecular medicine reports · 2021Article
- Transcriptional response of human articular chondrocytes treated with fibronectin fragments: an in vitro model of the osteoarthritis phenotype.Osteoarthritis and cartilage · 2021Article
- CREB Ameliorates Osteoarthritis Progression Through Regulating Chondrocytes AutophagyFrontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposesOsteoarthritis (OA) is a common joint disease characterized by the degradation of articular cartilage and joint inflammation. Interleukin-1ß induces P38/cAMP response element binding protein (CREB) pathway activation, resulting in increased expression of matrix metallopeptidase-13 (MMP13) in chondrocytes. However, the role of the P38/CREB/MMP13 axis is unclear in the progression of OA. In this study, we aimed to answer the following questions: (1) how does the P38/CREB/MMP13 axis in cartilage from patients with OA compare with control specimens? (2) Can the P38 agonist anisomycin (ANS) induce mouse OA? MATERIALS AND
methodsSurgical specimens of human cartilage were divided into OA and control groups. Surgical specimens of mouse cartilage were divided into control and ANS-induced groups. Safranin O staining of the cartilage tissues was performed to evaluate the extracellular matrix. Reverse transcription-polymerase chain reaction was performed using these tissues to investigate messenger RNA expressions of type II collagen, aggrecan, MMP13, and ADAM metallopeptidase with thrombospondin type 1 motif 5. Phosphorylated (p)-P38, p-CREB, and MMP13 were evaluated by Western blot analysis. Anisomycin was used to activate P38, and p-P38, p-CREB, and MMP13 were evaluated by immunofluorescence and Western blot analysis.
resultsSafranin O staining showed that the extracellular matrix degraded in humans with OA and ANS-induced mouse cartilage samples. The expressions of p-P38, p-CREB, and MMP13 were all upregulated in osteoarthritic cartilage or anisomycin-induced chondrocytes, suggesting that the P38/CREB/MMP13 axis may play a role in the progression of OA.
conclusionsThe P38/CREB/MMP13 axis is active in osteoarthritic chondrocytes and may cause the degeneration of cartilage. Effective new therapy directed against this pathway could be developed.
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