自噬在肺动脉高压发生和发展中的调节作用

肺动脉高压是一类多病因导致肺血管重构、肺动脉阻力进行性增高的慢性疾病，其发病机制错综复杂。近年研究发现，自噬作为真核生物维持细胞内环境稳定的一种自我保护机制，参与多种类型肺动脉高压的发生和发展。自噬通过调节肺血管壁细胞的生存、凋亡以及血管活性物质和炎症介质分泌等病理变化影响肺血管稳态。一些能调节自噬活性的药物对肺动脉高压的治疗有很好的临床应用价值。本文综述了自噬在肺动脉高压发生和发展中的调节作用，为临床治疗提供新的思路。
Abstract: 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. Key words: Hypertension, pulmonary/pathology Autophagy/physiology Pulmonary artery/pathology Endothelium, vascular/drug effects Review