氧化应激调控细胞外基质代谢的研究进展

摘要

The generation of reactive oxygen species increase and the ability of anti-oxidation decrease when the organism suffer from noxious stimulus, which can lead to oxidation-antioxidant imbalance and result in oxidative stress. Oxidative stress participate in the pathological process of ECM metabolism disorders of bones and joints, cardiovascular system and many other organs through TGF-β1/Smad3, MAPK/ERK, PI3K/Akt, JAK/STAT, Nrf2/ARE or Wnt/β-catenin pathways. The correlations between oxidative stress and ECM metabolism reported less at present.%机体遭受有害刺激引起活性氧簇(ROS)生成增加或抗氧化防御能力减弱时,可导致氧化-抗氧化失衡,引起氧化应激(OS).OS可通过激活TGF-β1/Smad3、MAPK/ERK、PI3K/Akt、JAK/STAT、Nrf2/ARE、Wnt/β-catenin等一系列信号通路及其相关效应因子,造成组织器官细胞外基质(ECM)成分代谢及相关因子表达异常,参与骨关节、心血管、肝、肾等组织器官ECM代谢异常疾病的发生发展.目前关于OS和盆腔器官脱垂的关联性的报道较少.