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Syntenin-1-mediated arthritogenicity is advanced by reprogramming RA metabolic macrophages and Th1 cells

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Once 2,4-D enters the human body, it is metabolised and excreted mainly in the urine, either unchanged or as biologically active and often toxic metabolites 22,23

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Thus, oxidative stress, which is the result of an imbalance between prooxidants and antioxidants towards the former due to excessive production of free radicals and/or a decrease in the activity of antioxidant defense, underlies the pathogenesis of many diseases and its study in modeling experimental pathology serves as a fundamental basis for clinical research