内皮细胞凋亡与肺动脉高压

Endothelial cell apoptosis and pulmonary arterial hypertension

随着肺动脉高压研究的不断深入,肺血管内皮细胞凋亡在肺动脉高压形成过程中的重要作用被逐步认识。多种疾病和环境因素导致肺血管内皮损伤、内皮细胞凋亡增加、功能障碍,从而促进肺动脉平滑肌细胞和成纤维细胞增殖、肺动脉重构和血栓形成;肺血管内皮细胞凋亡还诱导产生凋亡抵抗表型的内皮细胞过度增殖,形成丛样病变和肺血管闭塞,最终导致严重肺动脉高压。因而在肺动脉高压发生发展的不同时期,调控肺血管内皮细胞凋亡可能是预防和治疗肺动脉高压的一种新策略。

With the deeply researching on pulmonary arterial hypertension （PAH）, it is gradually clear that pulmonary vascular endothelial cell apoptosis plays a critical role in the forming and progressing of PAH. A wide variety of diseases and environmental factors can induce vascular endothelium injury, endothelial cell ap- optosis and endothelial dysfunction. In situ thrombosis, apoptosis of pulmonary vascular endothelial cells stimulates proliferation of pulmonary vascular smooth muscle cells and fibroblasts, remodelling of pulmonary vascular. And subsequent hyperproliferation of apoptosis-resistant endothelial cells induced by endothelial cells apoptosis leads to the formation of plexiform lesions and the obliteration of vascular lumina, and eventually causes severe PAH. Therefore, regulating pulmonary vascular endothelial cell apoptosis may serve as a new strategy for prevention and treatment of PAH.