Department of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, People's Republic of China.
Free Radic Biol Med. 2009 Oct 1;47(7):891-905. doi: 10.1016/j.freeradbiomed.2009.06.033. Epub 2009 Jul 3.
Psoriasis is a chronic immune-mediated hyperproliferative inflammatory skin disease in which a cytokine network concept is well established. Skin is a major target of oxidative stress mainly due to reactive oxygen species (ROS) originating from the environment and skin metabolism itself. Although endogenous antioxidants attenuate the harmful effects of ROS, increased or prolonged presence of free radicals can override ROS defense mechanisms and mediate numerous cellular responses that contribute to the development of a variety of skin disorders, including psoriasis. Regarding psoriasis, antioxidant strategies have proven to be beneficial therapeutics. The cellular signaling pathways such as mitogen-activated protein kinase/activator protein 1, nuclear factor kappaB, and Janus kinase-signal transducers and activators of transcription are known to be redox sensitive and proven to be involved in the progress of psoriasis. This review summarizes the current knowledge of the role of the redox system in regulating these signaling pathways related to the pathogenesis of psoriasis.
银屑病是一种慢性免疫介导的过度增生性炎症性皮肤病，其中细胞因子网络概念已经得到很好的建立。皮肤是氧化应激的主要靶点，主要是由于来自环境和皮肤代谢本身的活性氧（ROS）。尽管内源性抗氧化剂减轻了 ROS 的有害影响，但自由基的增加或延长存在可能会超过 ROS 防御机制，并介导许多细胞反应，导致多种皮肤疾病的发展，包括银屑病。关于银屑病，抗氧化策略已被证明是有益的治疗方法。丝裂原活化蛋白激酶/激活蛋白 1、核因子 kappaB 和 Janus 激酶信号转导物和转录激活物等细胞信号通路已知是氧化还原敏感的，并已被证明参与银屑病的进展。本综述总结了氧化还原系统在调节与银屑病发病机制相关的这些信号通路中的作用的最新知识。
