ArticleScientific reports2026
YKL-40 alleviates the TNF-α-Induced chondrocyte injury in osteoarthritis in vitro.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
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11 authors.
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Abstract
Osteoarthritis (OA) is a degenerative joint disease with high global prevalence, and YKL-40 is an important factor related to the pathological process of OA. Increased levels of YKL-40 exert a protective influence against TNF-α-induced apoptosis in chondrocytes, thereby enhancing chondrocyte survival and activation, while counteracting TNF-α-driven expression of specific inflammatory mediators such as S100A8/A9.This study aims to evaluate the role and molecular mechanism of YKL-40 on chondrocytes in OA and provide a potential therapeutic avenue requiring further validation. A meta-analysis compared serum YKL-40 and TNF-α levels between OA patients and healthy controls. In vitro experiments examined the effects of YKL-40 on TNF-α-induced OA chondrocytes, assessing proliferation, differentiation, apoptosis, and inflammatory pathways. Meta-analysis revealed significantly elevated serum levels of YKL-40 and TNF-α in osteoarthritis (OA) patients compared to healthy controls. In vitro, TNF-α (10 ng/mL) induced extracellular matrix (ECM) degradation in chondrocytes, significantly reducing glycosaminoglycan (GAG) and type II collagen content. This degradation was effectively rescued by YKL-40 (100 ng/mL). RNA sequencing identified differentially expressed genes in TNF-α-treated chondrocytes, enriched in pathways like IL-17 and NF-κB signaling. YKL-40 treatment reversed the expression of key genes altered by TNF-α. Crucially, these differentially expressed genes (including S100A8/A9, ISG15, CDSN, BAAT, PTPN4, NPTX1, SMARCA1) were validated in independent OA cartilage and synovium GEO datasets. Protein-protein interaction (PPI) networks highlighted central genes within treatment groups. Western blotting confirmed YKL-40 counteracted TNF-α-induced NF-κB pathway activation (reduced p65 and IκBα phosphorylation) and modulated key targets (S100A8/A9, ASB7, ZFPM2), consistent with qRT-PCR data. YKL-40 is a promising biomarker and therapeutic target for OA. Its interplay with TNF-α provides a molecular basis for novel therapies targeting chondrocyte dysfunction, guiding future translational research.
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