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Lu Xiaofeng, Luo Jingying. Department of Dermatology, Affiliated Hospital of Guilin Medical University, Guilin 541001, China Corresponding author: Luo Jingying, Email: luojingying2005@aliyun.com ��Abstract�� Systemic 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.

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