Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: Central role of nitric oxide in the pathogenesis of rheumatoid arthritis and systemic lupus erythematosus. | Nagy et al. Arthritis Research Therapy 2010 12 210 http content 12 3 210 REVIEW Central role of nitric oxide in the pathogenesis of rheumatoid arthritis and systemic lupus erythematosus Gyorgy Nagy - 2 Agnes Koncz2 Tiffany Telarico3 David Fernandez3 Barbara Érsek2 Edit Buzás2 and András Perl3 Abstract Nitric oxide NO has been shown to regulate T cell functions under physiological conditions but overproduction of NO may contribute to T lymphocyte dysfunction. NO-dependent tissue injury has been implicated in a variety of rheumatic diseases including systemic lupus erythematosus SLE and rheumatoid arthritis RA . Several studies reported increased endogenous NO synthesis in both SLE and RA and recent evidence suggests that NO contributes to T cell dysfunction in both autoimmune diseases. The depletion of intracellular glutathione may be a key factor predisposing patients with SLE to mitochondrial dysfunction characterized by mitochondrial hyperpolarization ATP depletion and predisposition to death by necrosis. Thus changes in glutathione metabolism may influence the effect of increased NO production in the pathogenesis of autoimmunity. Basic functions of nitric oxide Nitric oxide NO is a short-lived signaling molecule that plays an important role in a variety of physiologic functions including the regulation of blood vessel tone inflammation mitochondrial functions and apoptosis 1 2 . NO was originally identified as endothelium-derived relaxant factor based on the observations of Furchgott and Zawadzki 3 . They observed that acethylcholine-induced blood vessel relaxation occurred only if the endothelium was intact. Some years later the endothelium-derived relaxant factor was identified as NO 4 . NO is synthesized from L-arginine by NO synthetases NOSs neuronal NOS nNOS inducible Correspondence gyorgyngy@ Department of Rheumatology Semmelweis University Medical School Árpád fejedelem út 7 Budapest Hungary Full list of author information
