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肺动脉高压分子机制的研究进展 被引量：3

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摘要 肺动脉高压（pulmonary arterial hypertension,PAH）是以肺血管阻力进行性升高,和右心功能进行性衰竭为主要特征的病理过程,是很多心、肺血管疾病发生、发展的重要病理生理基础.最近的临床实验、基础研究中发现[1],一些细胞因子、信号通路、基因表达、离子通道功能等发生改变后,血管内大量异常增殖反应,导致了不可逆性肺血管的重构,肺动脉高压形成的结局,而且它们之间并不是独立的,有很多的相互作用.这里,就其分子机制综述如下.
作者 陈普文 黄石安
机构地区 湛江广东医学院附属医院
出处 《心肺血管病杂志》 CAS 2014年第1期130-132,共3页 Journal of Cardiovascular and Pulmonary Diseases
关键词 肺动脉高压 发病机制 血管重构
分类号 R56 [医药卫生—呼吸系统]
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参考文献34

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二级参考文献43

共引文献71

同被引文献18

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  • 10陈明,方少兵,刘衍斌,李桔莲,程起,周小英,相广财.实时三维超声心动图左心房容积指数评价2型糖尿病患者左心房功能[J].中国医药导报,2013,10(19):109-111. 被引量：3

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心肺血管病杂志
2014年 第1期

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