Lyu Dandan, Ying Kejing
Department of Respiratory Medicine, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou 310016, China.
Zhejiang Da Xue Xue Bao Yi Xue Ban. 2018 May 25;47(2):207-212. doi: 10.3785/j.issn.1008-9292.2018.04.16.
Pulmonary arterial hypertension (PAH) is a multi-etiological chronic disease characterized by a progressive elevation in pulmonary resistance and vascular remodeling. Its pathogenesis is complicated. Recently, emerging researches suggest that autophagy, as a self-protection mechanism maintaining the intracellular environment homeostasis in eukaryotes, participate in the occurrence and development of various types of PAH. Autophagy can regulate the survival, apoptosis of pulmonary vascular wall cells and secretion of vasoactive substances and inflammatory cytokines, thus influencing pulmonary vascular homeostasis. Some drugs based on regulating autophagy activity can effectively improve the prognosis of PAH. In this article, the regulatory role of autophagy on the development of pulmonary hypertension is reviewed to provide insight into PAH and its treatment.
肺动脉高压（PAH）是一种多病因的慢性疾病，其特征是肺血管阻力进行性升高和血管重塑。其发病机制复杂。最近，新出现的研究表明，自噬作为真核生物中维持细胞内环境稳态的一种自我保护机制，参与了各种类型PAH的发生和发展。自噬可以调节肺血管壁细胞的存活、凋亡以及血管活性物质和炎性细胞因子的分泌，从而影响肺血管稳态。一些基于调节自噬活性的药物可以有效改善PAH的预后。本文综述了自噬对肺动脉高压发展的调节作用，以期为PAH及其治疗提供见解。
