ArticleIrish journal of medical science2026
Crosstalk between autophagy and ferroptosis related genes in osteoarthritis: insights from transcriptomic and in vitro analyses.
Article in Irish journal of medical science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Research progress of cuproptosis, ferroptosis, apoptosis, and autophagy in knee osteoarthritis.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
- Erratum issued
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOsteoarthritis (OA) is a prevalent musculoskeletal disorder characterized by progressive articular cartilage degradation, involving complex interactions between inflammatory and metabolic factors. Both autophagy and ferroptosis are key cellular processes implicated in OA pathogenesis, but their potential interplay remains poorly understood.
aimsThis study aimed to explore the transcriptional crosstalk between autophagy- and ferroptosis-related genes in OA.
methodsWe analyzed the gene expression dataset GSE207881, comprising 6 healthy and 59 OA cartilage samples, to identify differentially expressed genes (DEGs). These were intersected with established ferroptosis (from FerrDb) and autophagy (from HAMDB) gene sets, yielding 120 ferroptosis-related and 239 autophagy-related DEGs. Functional enrichment, protein-protein interaction (PPI) network, and correlation analyses were performed. Key bioinformatic predictions were validated in vitro using a TNF-α-induced inflammatory model in C28/I2 chondrocytes, assessed via qPCR, proliferation, viability, and senescence assays.
resultsWe identified significant co-expression networks linking ferroptosis and autophagy pathways. Functional annotations highlighted shared enrichment in oxidative stress, inflammatory response, and cellular homeostasis pathways. Core hub genes from both processes showed strong transcriptional coordination, with the most significant correlations observed between ferroptosis-related genes (ATF3, ACSL1) and autophagy-related genes (IL6, NFKBIA). In the TNF-α-induced chondrocyte model, these key genes were concordantly dysregulated, and their significant positive correlations were confirmed, reinforcing their co-regulatory relationship in an OA-relevant inflammatory context. These findings reveal a coordinated transcriptional program between autophagy and ferroptosis pathways during early OA pathogenesis.
conclusionThe study identifies specific hub genes as potential interactive nodes, providing novel insights into the molecular mechanisms of chondrocyte dysfunction and highlighting candidate targets for future therapeutic investigation.
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