风湿病的氧化还原发病机制

Olivia T Laniak, T. Winans, Akshay Patel, Joy Park, Andras Perl
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摘要

尽管自身免疫性风湿病是一些最广为人知的发病机制,但其发病机制尚未完全明了。细胞免疫系统的过度激活和自身抗体的特征性发展与氧化应激有关。典型的临床表现,如关节肿胀和畸形以及皮肤和内脏器官的炎症,也直接或间接地与氧化还原机制有关。氧化应激在产生和抑制方面的差异为风湿性疾病病理的广泛多样性提供了令人信服的证据,并解释了这些疾病的一些共同诱因和不协调表现。越来越多的证据表明,氧化还原机制在发病机制中的作用提供了一系列新的潜在治疗靶点。在此,我们将探讨氧化应激的产生机制,探索其在自身免疫和终末器官损伤中的作用,并讨论各种风湿性疾病如何表现出独特的特征,从而为治疗干预提供靶点。
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Redox Pathogenesis in Rheumatic Diseases.
Despite being some of the most anecdotally well-known roads to pathogenesis, the mechanisms governing autoimmune rheumatic diseases are not yet fully understood. The overactivation of the cellular immune system and the characteristic development of autoantibodies have been linked to oxidative stress. Typical clinical manifestations, such as joint swelling and deformities and inflammation of the skin and internal organs, have also been connected directly or indirectly to redox mechanisms. The differences in generation and restraint of oxidative stress provide compelling evidence for the broad variety in pathology among rheumatic diseases and explain some of the common triggers and discordant manifestations in these diseases. Growing evidence of redox mechanisms in pathogenesis has provided a broad array of new potential therapeutic targets. Here, we explore the mechanisms by which oxidative stress is generated, explore its roles in autoimmunity and end-organ damage, and discuss how individual rheumatic diseases exhibit unique features that offer targets for therapeutic interventions.
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