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作 者:张秀莉 李万成[2] ZHANG Xiuli;LI Wancheng(The First Affiliated Hospital of Chengdu Medical College,Chengdu 610500,China;Department of Respiratory Medicine, the First Affiliated Hospital of Chengdu Medical College, Chengdu 610500, China)
机构地区:[1]成都医学院第一附属医院,成都610500 [2]成都医学院第一附属医院呼吸内科,成都610500
出 处:《生命的化学》2018年第2期236-240,共5页Chemistry of Life
摘 要:肺纤维化(pulmonary fibrosis,PF)是许多肺损伤的共同过程,病理表现为肌成纤维细胞的大量集聚,细胞外基质的沉积。近年来研究表明,转化生长因子β1(transforming growth factor-β1,TGF-β1)/Smad通路在肺纤维化中有重要作用。核转录共抑制因子SnoN(Ski-related novel protein N)能通过Smads蛋白抑制TGF-β1信号通路从而调节肺纤维化的发生发展。本文就SnoN在肺纤维化TGF-β1/Smad通路中的作用作一综述,为治疗肺纤维化找到新方向。Pulmonary fibrosis is a common process of many lung injuries, and the pathological manifestations are the accumulation of myofibroblasts and the deposition of extracellular matrix. Recent studies have shown that the transformation growth factor β1/Smad pathway plays an important role in pulmonary fibrosis. SnoN can regulate the development of pulmonary fibrosis by inhibiting TGF-β 1 signaling pathway through Smads. This article reviews the role of SnoN in the TGF-β1/Smad pathway in pulmonary fibrosis, and finds a new direction for the treatment of pulmonary fibrosis.
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