作者：崔志峰，孙佳伟，刘美洋，宫小薇，袁雅冬

单位：

050000河北省石家庄市，河北医科大学第二医院呼吸与危重症医学科

Units：

Department of Respiratory and Critical Care Medicine, the Second Hospital of Hebei Medical University, Shijiazhuang 050000,China

关键词：

肺动脉高压；线粒体；线粒体功能障碍

Keywords：

Pulmonary arterial hypertension; Mitochondrion; Mitochondrial dysfunction

CLC：

DOI：

10.12114/j.issn.1008-5971.2022.00.165

Funds：

河北省重点研发计划项目（21377701D）

摘要：

肺动脉高压在病理上表现为一种增殖性疾病。研究显示，线粒体功能障碍参与肺血管及右心室的重塑。线粒体功能障碍涉及三羧酸循环、电子呼吸链、线粒体膜电位、线粒体钙储存、线粒体动力学、线粒体自噬以及线粒体生物发生等。线粒体以上各方面的异常均参与了肺动脉高压的形成。因此，恢复线粒体功能可能成为治疗肺动脉高压的新策略。本文主要综述了线粒体功能障碍在肺动脉高压形成中的作用机制。

Abstract：

Pulmonary hypertension is a proliferative disease pathologically. Studies have shown that mitochondrial dysfunction is involved in remodeling of pulmonary vessels and right ventricle. Mitochondrial dysfunction involves the tricarboxylic acid cycle, electronic respiratory chain, mitochondrial membrane potential, mitochondrial calcium storage, mitochondrialdynamics, mitochondrial autophagy, mitochondrial biogenesis and so on. The abnormalities of the above aspects of mitochondria are involved in the formation of pulmonary hypertension. Therefore, restoring mitochondrial function may be a new strategy totreat pulmonary hypertension. This paper reviewed the mechanisms of mitochondrial dysfunction in the formation of pulmonaryhypertension.

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