| Autor: |
Bryda, Jarosław, Wątroba, Sławomir |
| Předmět: |
|
| Zdroj: |
Journal of Pre-Clinical & Clinical Research; 2018, Vol. 12 Issue 4, p129-134, 6p |
| Abstrakt: |
Introduction. Rheumatoid arthritis (RA) is a chronic, systemic disease of connective tissue with autoimmune background. There is a lack of knowledge about the direct pathophysiological cause of RA formation. The involvement of lipoxygenase (LOX) in arachidonic acid (AA) metabolism can have a significant impact on the occurrence of RA. Lipid mediators play a significant role, inducing structural and metabolic changes in cells that initiate the activation of proinflammatory pathways and immune responses. Objective. The purpose of this review is to analyze the involvement of LOX in the etiopathogenesis of RA, with particular emphasis on 5-LOX and 15-LOX, as well as the characteristics of LOX enzymatic activity and identification of the role of AA metabolites in the inflammatory reaction process. State of knowledge. The effects of oxidative activity of LOX and dysfunctions of intracellular antioxidant systems lead to disturbance of redox homeostasis. The observed consequence of these phenomena are aberrations in the functioning of the immune system and accompanying inflammation. In RA studies, increased activity of 5-LOX and its reaction products was observed, such as leukotrienes B4 (LTB4) and 5-hydroxyeicosatetraenoic acid (5-HETE) in patients. A significant influence on the progression of RA is also associated with overexpression of 15-LOX, which leads to inhibition of chondrocyte proliferation and their apoptosis. Conclusion. The activity of the oxidative enzyme LOX is involved in the formation of lipid mediators responsible for inducing inflammation. The effects of the action of LOX may be disorders of the immune system that contribute to the development of RA. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
|
