Oxidative Stress in Autoimmune Rheumatic Diseases

Rheumatic diseases constitute a group of non-communicable diseases characterized by chronic inflammation. The most common autoimmune rheumatic diseases (ARDs) are rheumatoid arthritis, psoriatic arthritis, systemic lupus erythematosus, myositis, Sjogren's syndrome and systemic scleroderma. These autoimmune disorders lead to joint destruction and adversely influence the human body systemically. One of their characteristics is comorbidity, since patients usually suffer also from other pathologies such as cardiovascular diseases and obesity. In addition, their treatment requires a combination of both biological and conventional pharmaceutical interventions as well as other parameters such as physical activity programs, nutrition, and the use of smart electronic devices. Therefore, the ARDs burden health systems worldwide. Apart from the physiological manifestations of ARDs, specific changes are observed at the cellular and molecular level. A common biochemical/molecular symptom of these diseases is oxidative stress. This condition leads to the disturbance of blood and tissue redox status due to the excessive production of free radicals. Given that free radicals are highly reactive moieties with strong oxidative capacity against biomolecules (i.e., proteins, lipids, DNA), they compromise the efficacy of the intrinsic antioxidant mechanisms and, finally, induce the disruption of redox homeostasis. However, there is no sufficient data linking the levels of redox status of patients with the progression of ARDs over time. Indeed, the onset and symptoms of ARDs are intertwined with the disruption of the patient redox homeostasis and the induction of oxidative stress. Concurrently, the absence of a completely effective pharmaceutical treatment emerges the need for the adoption of novel biomarkers for monitoring the severity of the symptoms and the evolution of ARDs in general. To that end, this study aims at first to investigate the blood redox status of patients with ARDs. T