Mechanistic elucidation of ferroptosis and ferritinophagy: implications for advancing our understanding of arthritis.

In recent years, the emerging phenomenon of ferroptosis has garnered significant attention as a distinctive mode of programmed cell death. Distinguished by its reliance on iron and dependence on reactive oxygen species (ROS), ferroptosis has emerged as a subject of extensive investigation. Mechanistically, this intricate process involves perturbations in iron homeostasis, dampening of system Xc-activity, morphological dynamics within mitochondria, and the onset of lipid peroxidation. Additionally, the concomitant phenomenon of ferritinophagy, the autophagic degradation of ferritin, assumes a pivotal role by facilitating the liberation of iron ions from ferritin, thereby advancing the progression of ferroptosis. This discussion thoroughly examines the detailed cell structures and basic processes behind ferroptosis and ferritinophagy. Moreover, it scrutinizes the intricate web of regulators that orchestrate these processes and examines their intricate interplay within the context of joint disorders. Against the backdrop of an annual increase in cases of osteoarthritis, rheumatoid arthritis, and gout, these narrative sheds light on the intriguing crossroads of pathophysiology by dissecting the intricate interrelationships between joint diseases, ferroptosis, and ferritinophagy. The newfound insights contribute fresh perspectives and promising therapeutic avenues, potentially revolutionizing the landscape of joint disease management.

Exploration of effective biomarkers and infiltrating Immune cells in Osteoarthritis based on bioinformatics analysis.

Osteoarthritis (OA) is a multi-factorial chronic joint disease mainly identified by synovial inflammation, cartilage damage, and degeneration. Our study applied bioinformatics analysis to uncover the immunity in OA and tried to explore the underlying immune-related molecular mechanism. First, OA-related gene-expression profiling data were retrieved from GEO database. Then, we analysed a series of datadata with using the xCell algorithm, GEO2R, enrichment analysis of SangerBox website, CytoHubba, ROC logistic regression and correlation analysis. Finally, Nine infiltrating immune cells with differential abundance between OA and normal samples were obtained. There were 42 IODEGs in OA, and their functions were associated with immune cells and corresponding biological processes. Moreover, 5 hub genes, including GREM1, NRP1, VEGFA, FYN and IL6R, were identified. Correlation analysis demonstrated that NRP1 was negatively associated with NKT cells, NRP1 and GREM1 were positively associated with aDC, VEGFA was positively associated with CD8+ naïve T cells, while VEGFA, FYN and IL6R were negatively associated with Macrophages M1. The 5 hub genes could be employed as effective diagnostic biomarkers for OA. In addition, they may participate in OA pathogenesis via interactions with infiltrating immune cells.