ArticleJournal of orthopaedic surgery and research2024
PDK4 inhibits osteoarthritis progression by activating the PPAR pathway.
Article in Journal of orthopaedic surgery and research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 15 citations in OpenAlex.
- Immune dysregulation in osteoarthritis: Mechanisms, biomarkers, and therapeutic opportunities.Journal of translational autoimmunity · 2026Review
- Integrated Multi-Omics Analysis and Experimental Validation Identify Acetylation-Related Genes as Potential Regulators in Osteoarthritis.Biomedicines · 2026Article
- Continuous low-intensity ultrasound influences the transcriptomic profile in M1 macrophages by downregulating inflammation and promoting M2-like markers.Scientific reports · 2026Article
- PSMB9 exacerbates chondrocyte injury in osteoarthritis via activation of the NF-κB pathway.Journal of orthopaedic surgery and research · 2026Article
- Immune cells with senescence-related transcriptional signatures orchestrate the inflammatory continuum in osteoarthritis synovium: a single-cell and machine learning study.Frontiers in immunology · 2026Article
- Ultrasound therapy inhibits knee osteoarthritis progression in rabbits by activating the PPARs pathway: a pilot study.Annals of medicine · 2025Article
- KLF5 aggravates osteoarthritis progression by inhibiting chondrocyte autophagy via transcriptional activation of PLK2.Scientific reports · 2025Article
- Moxibustion ameliorates abnormal subchondral bone remodeling by promoting ACSL1-mediated autophagy to degrade NLRP3 in osteoarthritis.Chinese medicine · 2025Article
- Evaluating Potential Therapeutic Targets and Drug Repurposing Based on the Esophageal Cancer Subtypes.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Rapamycin reveals neuropeptide Y as a regulator of senescence and inflammatory pathways in arthritis.Neuropeptides · 2025Article
- The Role ofBiomolecules · 2025Review
- Intermittent fasting reduces inflammation and joint damage in a murine model of rheumatoid arthritis: insights from transcriptomic and metagenomic analyses.BMC rheumatology · 2024Article
- Screening and validation of key genes associated with osteoarthritis.BMC musculoskeletal disorders · 2024Article
- Enhancing Cartilage Metabolism in Rats through a Novel Thermal Stimulation Technique with Photosensitizers.International journal of molecular sciences · 2024Article
- Characterizing mitochondrial features in osteoarthritis through integrative multi-omics and machine learning analysis.Frontiers in immunology · 2024Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundOsteoarthritis (OA) is a degenerative joint disease caused by the deterioration of cartilage. However, the underlying mechanisms of OA pathogenesis remain elusive.
methodsHub genes were screened by bioinformatics analysis based on the GSE114007 and GSE169077 datasets. The Sprague-Dawley (SD) rat model of OA was constructed by intra-articular injection of a mixture of papain and L-cysteine. Hematoxylin-eosin (HE) staining was used to detect pathological changes in OA rat models. Inflammatory cytokine levels in serum were measured employing the enzyme-linked immunosorbent assay (ELISA). The reverse transcription quantitative PCR (RT-qPCR) was implemented to assess the hub gene expressions in OA rat models. The roles of PDK4 and the mechanism regulating the PPAR pathway were evaluated through western blot, cell counting kit-8 (CCK-8), ELISA, and flow cytometry assays in C28/I2 chondrocytes induced by IL-1β.
resultsSix hub genes were identified, of which COL1A1, POSTN, FAP, and CDH11 expressions were elevated, while PDK4 and ANGPTL4 were reduced in OA. Overexpression of PDK4 inhibited apoptosis, inflammatory cytokine levels (TNF-α, IL-8, and IL-6), and extracellular matrix (ECM) degradation protein expressions (MMP-3, MMP-13, and ADAMTS-4) in IL-1β-induced chondrocytes. Further investigation revealed that PDK4 promoted the expression of PPAR signaling pathway-related proteins: PPARA, PPARD, and ACSL1. Additionally, GW9662, an inhibitor of the PPAR pathway, significantly counteracted the inhibitory effect of PDK4 overexpression on IL-1β-induced chondrocytes.
conclusionPDK4 inhibits OA development by activating the PPAR pathway, which provides new insights into the OA management.
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