摘要系统性硬皮病是一种自身免疫性疾病,其确切病因不明,可能与微血管病变、免疫反应、细胞外基质合成过多相关.近年来,有证据表明,氧化应激可能在系统性硬皮病的发生发展过程中起重要作用.一些学者提出,在系统性硬皮病发生的初始阶段,患者体内激活的成纤维细胞能产生大量的活性氧,使机体处于一种过度的氧化应激状态,在这一状态下,大量产生胶原蛋白Ⅰ,促使组织纤维化.将围绕氧化应激、氧化应激产物及其如何通过调节细胞因子表达、介导免疫反应等方面参与皮肤和各器官纤维化的过程进行概述.

abstractsSystemic scleroderma is an autoimmune disease.Its exact etiology remains unknown,and may be related to microvascular abnormalities,immune response and excessive extracellular matrix synthesis.In recent years,oxidative stress has been proved to play an important role in the occurrence and development of systemic scleroderma.Some scholars presume that activated fibroblasts can produce large amounts of reactive oxygen species (ROS) at the initial phase of systemic scleroderma in patients,which makes the human body in a state of excessive oxidative stress.Under this condition,type Ⅰ collagen protein is synthesized in large amounts,which then leads to tissue fibrosis.In this review,the authors summarize oxidative stress,oxidative stress products and how they participate in the fibrosis of skin and other organs through regulating cytokine expressions and mediating immune reactions.