氧化应激调控细胞外基质代谢的研究进展
汤剑明 洪莉[摘要] 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。
[关键词] 氧化应激;细胞外基质;活性氧簇;纤维化
[中图分类号] R713 [文献标识码] A [文章编号] 1673-7210(2016)02(a)-0036-05
Research advances in regulation of extracellular matrix metabolism by oxidative stress
TANG Jianming HONG Li
Department of Gynecology and Obstetrics, Renmin Hospital of Wuhan University, Hubei Province, Wuhan 430060, China
[Abstract] 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. ......
您现在查看是摘要页,全文长 18704 字符。