金属硫蛋白在肺动脉高压形成中的机制研究进展

Research Progress in Mechanism of Metallothionein in Formation of Pulmonary Artery Hypertension

肺动脉高压(PAH)是一种罕见的进行性疾病,是由内皮功能障碍和肺动脉平滑肌细胞及成纤维细胞不受控制的增殖而导致的肺小动脉闭塞,涉及多种因子或蛋白质,目前尚不清楚这些因子/蛋白质确切的作用机制。线粒体调节在PAH形成的病理生理学中起到重要作用。金属硫蛋白(MTs)参与细胞增生和血管收缩,稳定内环境,研究MTs在PAH机制形成的发展,有助于更好地理解PAH形成的病理生理学,对肺血管功能具有临床意义,并有助于确定适合药物干预的可能靶点及途径。

Pulmonary artery hypertension(PAH)is a rare progressive disease characterized by pulmonary arteriole occlusion caused by endothelial dysfunction and uncontrolled proliferation of pulmonary artery smooth muscle cells and fibroblasts,involving a variety of molecular factors or proteins,and the exact action mechanism of these factors/proteins is still not clear.Mitochondrial regulation plays an important role in the pathophysiology of PAH.Metallothioneins(MTs)are involved in cell proliferation and vasoconstriction and internal environment stablization.Studying the development of MTs in the formation of PAH is helpful to better understand the pathophysiology,which is of clinical significance to pulmonary vascular function and is helpful to determine the possible targets and pathways of the drug intervention.