活性氧引起缺氧诱导因子1活化参与肺动脉高压血管重塑的分子机制  

Molecular Mechanism of Hypoxia-inducible Factor-1 Activation Induced by Reactive Oxygen Species in Vascular Remodeling of Pulmonary Hypertension

作　　者：薛进华[1,2] 叶超 毛露 Dirk Hermann 陈艾东 XUE Jinhua;YE Chao;MAO Lu;Dirk Hermann;CHEN Aidong(Research Center for Cardiovascular and Cerebrovascular Diseases,Gannan Medical College,Ganzhou 341000,Jiangxi,China;Center for Neurobiology,Duisburg-Essen University,Essen 45122,Germany;Key Laboratory of Targeting Interventions for Cardiovascular Diseases,Nanjing Medical University,Nanjing 211166,Jiangsu,China;Zhongda Hospital Affiliated to Southeast University,Southeast Medical University,Nanjing 210096,Jiangsu,China)

机构地区：[1]心脑血管疾病研究中心赣南医学院,江西赣州341000 [2]神经生物学研究中心杜伊斯堡-埃森大学,德国埃森45122 [3]心血管疾病靶向干预重点实验室南京医科大学,江苏南京211166 [4]东南大学附属中大医院东南医科大学,江苏南京210096

出　　处：《心血管病学进展》2020年第8期844-846,共3页Advances in Cardiovascular Diseases

基　　金：国家自然科学基金面上项目(31571168,81571246);国家公派留学基金(20173059);中国博士后基金(2016M591750,2017T100320)。

摘　　要：肺动脉高压的特点是血管收缩和血管平滑肌细胞增生,导致肺动脉血管的病理性重塑.活性氧介导缺氧诱导因子1的活化,通过一系列的下游细胞信号,引起肺血管的异常调节,造成管壁肥大和增厚,在肺动脉高压的血管重塑中起关键作用.肺动脉高压时,针对活性氧和缺氧诱导因子1的干预,以调节氧化还原信号为中心的治疗方法,有望成为本病治疗新的策略和重要靶点,现就此做一详细阐述.Pulmonary hypertension(PH)is characterized by vasoconstriction and proliferation of vascular smooth muscle cells,leading to pathological remodeling of pulmonary arteries.ROS mediates the activation of hypoxia-inducible factor-1(HIF-1).Through a series of downstream cell signals,it causes abnormal regulation of pulmonary vessels,resulting in hypertrophy and thickening of the vessel wall,which plays a key role in the vascular remodeling of PH.For the intervention of ROS and HIF-1 in PH,the treatment method centering on the regulation of redox signal is expected to become a new strategy and an important target for the treatment of this disease.This paper will elaborate on these in detail.

关 键 词：肺动脉高压 活性氧 缺氧诱导因子1 血管重塑 

分 类 号：R544.1[医药卫生—心血管疾病]