代谢重编程在肺动脉高压中的研究进展  

Metabolic reprogramming in pulmonary hypertension

作　　者：张若旸 刘杰[1] 孙英[1] 王炜[1] 王辰[2] Zhang Ruoyang;Liu Jie;Sun Ying;Wang Wei;Wang Chen(Department of Immunology,School of Basic Medical Sciences,Capital Medical University,Beijing 100069,China;Chinese Academy of Medical Sciences&Peking Union Medical College,Beijing 100730,China)

机构地区：[1]首都医科大学基础医学院免疫学系,北京100069 [2]中国医学科学院,北京协和医学院,北京100730

出　　处：《中华结核和呼吸杂志》2022年第3期313-317,共5页Chinese Journal of Tuberculosis and Respiratory Diseases

基　　金：国家自然科学基金(81770049);首都医科大学科研培育基金(PYZ19065)。

摘　　要：肺动脉高压是指由多种临床原因引起的肺动脉压力异常升高的病理生理状态,然而其发病机制还不完全清楚。肺血管结构细胞(平滑肌细胞、内皮细胞及成纤维细胞等)和免疫细胞(巨噬细胞等)中发生的代谢重编程被认为是肺动脉高压发病过程中的重要机制,后者介导了肺血管重塑并导致肺动脉高压。已有许多研究发现了肺动脉高压中复杂的代谢重编程现象,并基于代谢通路靶点进行药物干预。本文将对代谢重编程在肺动脉高压中的作用研究进行综述。Pulmonary hypertension is a pathophysiological disorder with elevated pulmonary artery pressures that may involve multiple clinical conditions,yet the mechanism of pulmonary hypertension remains unclear.Metabolic reprogramming of structural cells(smooth muscle cells,endothelial cells,fibroblasts etc.)and immune cells(macrophages etc.)is a hallmark of pulmonary hypertension and leads to pulmonary vascular remodeling.Many studies have investigated the metabolic reprogramming in pulmonary hypertension and some potential therapeutic targets have been developed.In this review,recent work on metabolic programming in pulmonary hypertension is summarized.

关 键 词：病理生理状态 肺动脉高压 肺动脉压力 肺血管重塑 代谢通路 临床原因 内皮细胞 免疫细胞 

分 类 号：R544.1[医药卫生—心血管疾病]