肺动脉高压的治疗药物虽然取得一定进步，包括一氧化氮、前列环素类似物等药物的应用，一定程度上缓解了病程的进展，但并从根本上消除疾病的影响。最新的病理学研究提示，肺动脉高压的病理发生发展过程中核心是血管内皮功能障碍和平滑肌增生性改变。线粒体是最重要的细胞凋亡途径之一，研究证实线粒体融合蛋白-2（mitofusin-2，Mfn2）具有很强的抑制血管平滑肌增生、促进其凋亡的作用，能够潜在的抑制肺动脉纤维化生。内皮祖细胞与成熟内皮细胞相比，在功能上尚处于未分化完全阶段，具有更强的增殖能力，更好的生长扩增和分泌血管新生因子的能力，促进血管新生。因此我们创意利用基因学手段，从肺动脉高压发生的核心环节，利用转染Mfn2基因的内皮祖细胞，自体移植，从而抑制肺动脉纤维化生，促进肺微血管新生，达到治疗肺动脉高压的目的。

There is still no radical treatment of pulmonary hypertension(PH),although various therapies of PH have advanced in the past few decades. The latest pathological studies indicated that endothelial dysfunction and prominent proliferation of pulmonary arterial smooth muscle cells(PASMC) are invloved in the key point of PH. Mitochondria is one of the most important cell apoptosis pathway,and mitofusin-2(Mfn2) exerts strong effects on inhibition of proliferation and promotion of apoptosis of PASMC.Simultaneously,as the precursor of endothelium, endothelial progenitor cell(EPC) has greater generation potential into endothelial cells and angiogenesis. So we expect autologous implantation of EPC transfected by Mfn2 gene to treat PH by promoting endothelial repair and induce PASMC apoptosis from the pathological basis.