肺动脉成纤维细胞在低氧性肺动脉高压中的作用

Function of pulmonary arterial fibroblasts in hypoxic pulmonary hypertension

近年来肺动脉成纤维细胞（pulmonary arterial fibroblasts，PAF）在低氧性肺动脉高压病理过程中的作用得到重视。低氧可以诱导肺动脉成纤维细胞产生一系列表型的改变，如增殖增强、分泌蛋白的异常等。低氧还可以促进PAF与其他细胞相互作用，如平滑肌细胞、炎性细胞、循环纤维细胞等，从而进一步加速血管重塑及肺动脉高压的形成。PAF在低氧诱导下所发生的变化受多种机制的调控，包括多条信号通路、线粒体来源的活性氧簇调控及其他机制等。PAF在低氧性肺动脉高压中的作用及作用机制有待更深入的研究。

The role of pulmonary arterial fibroblasts （PAF） in the pathogenesis of hypoxic pulmonary hypertension has been recognized recently. Hypoxia could induce a series of phenotypic changes of PAF, such as increased proliferation and abnormal proteins secretion, ttypoxia could also promote the interaction of PAF with other cells, such as smooth muscle cells, inflammatory cells, circulating fibroblasts, which could accelerate the formation of vascular remodeling and pulmonary hypertension. The changes Of PAF under hypoxia might be conducted by a variety of mechanisms, including multiple signaling pathways involvement, active oxygen species derived from mitochondria and other mechanisms. The roles of PAF in hypoxic pulmonary hypertension and its mechanism need to be further studied.