The Regulatory Role of NRF-2 in Rheumatoid Arthritis

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Rheumatoid arthritis is a chronic inflammatory condition with an impact on the musculoskeletal system characterized by both synovial hyperplasia and bone degeneration. Rheumatoid arthritis is a systemic and auto-immune illness that results in polyarthritis, particularly in the bone joints. Although the cause is unknown, it is assumed to be a multi-factorial disorder with both inherited and environmental factors as perceived causative factors. Patients with rheumatoid arthritis have higher genetic and protein expression of nuclear factor erythroid 2-related factor 2/heme oxygenase 1 (Nrf-2/HO-1). Nuclear factor erythroid 2-related factor 2 (Nrf-2) is involved in the maintenance of inflammation as well as the regulation of adaptive and innate immune responses. Pro-inflammatory mediators are among the numerous agents involved in the development of arthritis. The reduced level of Nrf-2 is another important component in the pathogenesis of rheumatoid arthritis. Nrf-2 attaches to the antioxidant response element, which encodes antioxidant enzymes that inhibit the generation of free radicals and reactive oxygen species, resulting in a reduction in inflammation. The upregulation of Nrf-2 could be investigated as potential new therapeutic avenues for rheumatoid arthritis treatment. This chapter provides a thorough understanding of Nrf-2 mechanisms, which is a prerequisite for rheumatic illness clinical trials, and the developments in the management and treatments for rheumatoid arthritis. The activation of Nrf-2 could lead to the development of adjuvant medicines, which would boost cellular responses to other treatments. To facilitate the development of new therapeutic medicines, these new ideas associated with the Nrf-2 pathway must be explored.