ArticleClinical and translational medicine2026
DCLK1-dependent NF-κB activation mediates p-STAT3-induced osteoarthritis progression.
Article in Clinical and translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundOsteoarthritis (OA) is a widespread degenerative joint disorder marked by irreversible cartilage destruction. While signal transducer and activator of transcription 3 (STAT3) is recognised as a pivotal regulator in its pathogenesis, the downstream regulatory cascades of phosphorylated STAT3 (p-STAT3) in chondrocyte extracellular matrix (ECM) metabolism remain elusive. Our study sought to identify p-STAT3-mediated novel pathways driving OA.
methodsP-STAT3 expression was detected in human/mouse OA cartilage. Chondrocyte-specific STAT3 knockout mice (Stat3
resultsP-STAT3 was significantly upregulated in OA cartilage. STAT3 knockout ameliorated OA progression. Mechanistically, p-STAT3 directly bound the doublecortin-like kinase 1 (DCLK1) promoter to activate its transcription. DCLK1 interacted with IKKβ, promoting IKKβ phosphorylation and NF-κB activation, ultimately upregulating MMP13 and downregulating COL2A1.
conclusionsThis study identifies a novel p-STAT3/DCLK1/IKKβ/NF-κB axis that regulates cartilage matrix metabolism and OA progression, suggesting new therapeutic targets for OA intervention. KEY POINTS: Doublecortin-like kinase 1 (DCLK1) is identified as a novel phosphorylated signal transducer and activator of transcription 3 (p-STAT3) transcriptional target. A novel p-STAT3/DCLK1/IKKβ/NF-κB axis regulates chondrocyte extracellular matrix (ECM) metabolism and drives osteoarthritis progression. Genetic and pharmacological translational evidence validates the p-STAT3/DCLK1 axis as a prospective therapeutic target against osteoarthritis.
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