肺动脉内皮细胞炎症反应在低氧性肺动脉高压中的作用研究进展  

Research Progress on the Role of Inflammatory Response of Pulmonary Artery Endothelial Cells in Hypoxic Pulmonary Hypertension

作　　者：滕慧芳 秦仕虹 符代炎 TENG Huifang;QIN Shihong;FU Daiyan(Respiratory Five Department,the First Affiliated Hospital of Hunan Normal University/Hunan Provincial People's Hospital,Changsha 410000,China)

机构地区：[1]湖南师范大学附属第一医院湖南省人民医院呼吸五病区,湖南省长沙市410000

出　　处：《实用心脑肺血管病杂志》2023年第7期33-39,43,共8页Practical Journal of Cardiac Cerebral Pneumal and Vascular Disease

基　　金：湖南省自然科学基金——科卫联合项目(2022JJ70094);湖南省教育厅科学研究项目(20A298);长沙市科技计划项目(kq2004112)。

摘　　要：低氧性肺动脉高压(HPH)是一种由低氧引起的肺血管疾病,通常发生在各种肺部疾病引起的慢性低氧环境中,肺血管收缩和肺血管重塑是HPH最重要的致病过程,其可引起肺血管阻力升高,导致肺动脉压力升高,最终造成患者发生右心衰竭甚至死亡。HPH病理机制复杂,其中低氧、炎症反应导致的肺动脉内皮功能障碍是肺血管重塑的关键。本文就肺动脉内皮细胞及相关的炎症细胞、炎症因子在HPH中的作用做一综述,以期为HPH的诊疗和预防提供新的思路。Hypoxic pulmonary hypertension(HPH)is a pulmonary vascular disease caused by hypoxia and usually occurs in chronic hypoxia environments caused by various lung diseases.Pulmonary vasoconstriction and pulmonary vascular remodeling are the most important pathogenic processes in HPH,which can cause an increase in pulmonary vascular resistance,leading to an increase in pulmonary artery pressure and ultimately right heart failure and even death.The pathological mechanism of HPH is complex,and the dysfunction of pulmonary artery endothelium caused by hypoxia and inflammatory reactions is the key to pulmonary vascular remodeling.This article provides a review on the role of pulmonary artery endothelial cells,related inflammatory cells,and inflammatory factors in HPH,in order to provide new ideas for the diagnosis,treatment,and prevention of HPH.

关 键 词：肺动脉高压 低氧性肺动脉高压 内皮细胞 炎症 综述 

分 类 号：R541.5[医药卫生—心血管疾病]