期刊文献+

野百合碱诱导肺动脉高压模型的机制研究及潜在临床应用价值进展 被引量:2

Advanced mechanisms and potential clinical application value of monocrotaline-induced pulmonary artery hypertension animal model
下载PDF
导出
摘要 肺动脉高压(PAH)是以肺动脉压力和肺血管阻力升高为特征的致死性心血管疾病。野百合碱(MCT)引起的PAH病理特征和临床患者十分相似。MCT可以通过炎症反应、内皮途径以及调节肺动脉平滑肌细胞的增殖等因素诱导PAH的发生。因此本文对近几年MCT诱导PAH动物模型的作用机制以及在PAH新治疗药物靶点筛选中的应用进行简要综述。 Pulmonary artery hypertension(PAH)is a fatal cardiovascular disease characterized by increases in pulmonary artery pressure and pulmonary vascular resistance.The pathological features of PAH induced by monocrotaline(MCT)are similar to those of clinical patients.MCT-induced PAH through multiple factors including inflammatory response,endothelium pathway,and regulation of pulmonary artery smooth muscle cells proliferation,et al.Therefore,this article briefly reviews the advances molecular mechanism of the MCT-induced PAH and the exploration in the novel therapeutic targets by using this animal model in recent years.
作者 程筱涵 齐靖 白玉华 郑晓东 CHENG Xiaohan;QI Jing;BAI Yuhua;ZHENG Xiaodong(College of Pharmacy,Harbin Medical University(Daqing),Heilongjiang Province,Daqing163319,China;College of Basic Medical Sciences,Harbin Medical University(Daqing),Heilongjiang Province,Daqing163319,China)
出处 《中国医药导报》 CAS 2020年第27期40-43,共4页 China Medical Herald
基金 国家自然科学基金资助项目(31500936) 黑龙江省自然科学基金项目(C2017042) 中央支持地方高校发展人才培养支持计划-优秀青年人才支持项目。
关键词 肺动脉高压 野百合碱 信号通路 药物靶点 Pulmonary arterial hypertension Monocrotaline Signal pathway Drug target
  • 相关文献

参考文献2

二级参考文献54

  • 1荆志成.2010年中国肺高血压诊治指南[J].中国医学前沿杂志(电子版),2011,3(2):62-81. 被引量:117
  • 2McLaughlin VV. Looking to the future: a new decade of pulmonary arterial hypertension therapy. Eur Respir J 2011; 20: 262-9.
  • 3Mathew R. Pathogenesis of pulmonary hypertension: a case for caveolin-1 and cell membrane integrity. Am J PhysioI-Heart C 2014; 306: H15-25.
  • 4Rosanio S, Pelliccia F, Gaudio C, Greco C, Keylani AM, D'Agostino DC. Pulmonary arterial hypertension in adults: novel drugs and catheter ablation techniques show promise? Biomed Res Int 2014; 2014: 743868.
  • 5Zamanian RT, Kudelko KT, SungYK, de Jesus PerezV, Liu J, Spiekerkoetter E. Current clinical management of pulmonary arterial hypertension. Circ Res 2014; 115: 131-47.
  • 6Han C, Hong KH, Kim YH, Kim M J, Song C, Kim M J, et al. SMAD1 deficiency in either endothelial or smooth muscle cells can predispose mice to pulmonary hypertension. Hypertension 2013; 61: 1044-52.
  • 7Upton PD, Davies R J, Tajsic T, Morrell NW. Transforming growth factor- beta(l) represses bone morphogenetic protein-mediated Smad signaling in pulmonary artery smooth muscle cells via Smad3. Am J Resp Cell Mol 2013; 49: 1135-45.
  • 8Yang J, Davies R J, Southwood M, Long L, Yang X, Sobolewski A, et al. Mutations in bone morphogenetic protein type Ⅱ receptor cause dysregulation of Id gene expression in pulmonary artery smooth muscle cells: implications for familial pulmonary arterial hypertension. Circ Res 2008; 102: 1212-21.
  • 9Nishikawa-Takahashi M, Ueno S, Kario K. Long-term advanced therapy with bosentan improves symptoms and prevents deterioration of inoperable chronic thromboembelic pulmonary hypertension. Life Sci 2014; 118: 410-3.
  • 10Fontoura D, Oliveira-Pinto J, Tavares-Silva M, Leite S, Vasques-Novoa F, Mendes-Ferreira P, et al. Myocardial and anti-inflammatory effects of chronic bosentan therapy in monocrotaline-induced pulmonary hypertension. Rev Port Cardio12014; 33: 213-22.

共引文献17

同被引文献14

引证文献2

二级引证文献9

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部