ArticleJournal of inflammation research2026
Disulfidptosis-Induced Chondrocyte-Macrophage Crosstalk via GYS1/CCND1/NOD2 Axis Promotes Osteoarthritis Progression.
Article in Journal of inflammation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- Disulfidptosis: Mechanisms, evidence boundaries, and translational opportunities.Redox biology · 2026Review
- Disulfidptosis vs. Ferroptosis: A Comprehensive Review of SLC7A11-Mediated Metal Dyshomeostasis and Cell Death.Biomolecules · 2026Review
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: To investigate the potential role and underlying mechanisms of disulfidptosis, a novel form of regulated cell death, in the pathogenesis of degenerative osteoarthritis (OA), and to evaluate its association with M1-type macrophage infiltration and diagnostic biomarker potential. Methods: Human articular cartilage samples from OA patients and non-OA controls were analyzed using high-throughput RNA sequencing to identify disulfidptosis-related gene expression patterns. Immunohistochemical assays were performed to validate key molecular signatures in chondrocytes. Differentially expressed genes (DEGs) were screened to identify candidates linking disulfidptosis to M1 macrophage biology. Functional correlation analyses were conducted to explore gene-immune cell interactions. Glucose starvation was applied to induce disulfidptosis in ATDC5 chondrocyte line; a co-culture system with RAW264.7 macrophage cell line was established to validate their functional roles and underlying mechanisms. Results: OA chondrocytes exhibited a low-glucose metabolic state and elevated SLC7A11 (a cystine/glutamate transporter implicated in disulfidptosis) expression, consistent with a disulfidptosis signature, and showed increased immune infiltration of M1-type macrophages. Among the DEGs, Glycogen synthase 1 (GYS1) emerged as a key disulfidptosis-related gene directly regulating transcriptional programs in M1 macrophages. Functional analyses suggested that disulfidptosis in chondrocytes may indirectly promote M1 macrophage-mediated immune infiltration through cyclin D1 (CCND1) and nucleotide-binding oligomerization domain-containing protein 2 (NOD2), thereby contributing to OA progression. Conclusion: Disulfidptosis in chondrocytes is associated with M1 macrophage immune infiltration and could drive OA progression. Mechanism genes like GYS1/CCND1/NOD2 have diagnostic potential and could be novel biomarkers and therapeutic targets for OA. These findings highlight the translational potential of targeting disulfidptosis-related pathways to improve OA management and patient outcomes.
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