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氧化应激在硬皮病纤维化中作用的新见解。

New insights into the role of oxidative stress in scleroderma fibrosis.

作者信息

Gabrielli Armando, Svegliati Silvia, Moroncini Gianluca, Amico Donatella

机构信息

Dipartimento di Scienze Cliniche e Molecolari - Clinica Medica - Università Politecnica delle Marche, Ancona, Italy.

出版信息

Open Rheumatol J. 2012;6:87-95. doi: 10.2174/1874312901206010087. Epub 2012 Jun 15.

Abstract

Systemic sclerosis (Scleroderma - SSc) is a connective tissue disorder of unknown aetiology characterized by extensive fibrosis of the skin and visceral organs, by vascular abnormalities and immunological manifestations.Recent evidence suggest that the cellular redox state may play a significant role in the progression of scleroderma fibrosis. Mechanisms involved include an autoamplification circuit linking ROS, Ras and ERK 1-2 which in turn amplifies and maintains the autocrine loop made up by cytokines, growth factors and their cognate receptors.This review summarizes the recent progress on the role of oxidative stress in the pathophysiology of scleroderma and disorders characterised by organ fibrosis.

摘要

系统性硬化症(硬皮病 - SSc)是一种病因不明的结缔组织疾病,其特征为皮肤和内脏器官广泛纤维化、血管异常及免疫表现。最近的证据表明,细胞氧化还原状态可能在硬皮病纤维化进展中起重要作用。涉及的机制包括一个将活性氧(ROS)、Ras和细胞外信号调节激酶1 - 2(ERK 1 - 2)联系起来的自放大回路,该回路反过来又放大并维持由细胞因子、生长因子及其同源受体组成的自分泌环。本综述总结了氧化应激在硬皮病及以器官纤维化为特征的疾病病理生理学中作用的最新进展。

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