细胞自噬与肺纤维化疾病

肺纤维化是多种肺疾病常见的终末期病理学改变,其发生发展是由多种细胞、细胞因子、蛋白酶共同参与控制。研究表明,细胞自噬在肺部炎症和纤维化过程中发挥着重要作用,可以通过抑制炎性细胞因子和促纤维化因子的分泌、降解成纤维细胞中的胶原蛋白以及抑制上皮间质转化(epithelial-mesenchymal transition,EMT)过程,达到减轻肺纤维化的作用。本文就细胞自噬在特发性肺纤维化(IPF)、肺囊性纤维化(PCF)和矽肺所致肺纤维化(silicotic pulmonary fibrosis)中的作用及机制进行简要归纳,为今后工作提供参考。

Autophagy and pulmonary fibrosis

Pulmonary fibrosis is a common end-stage of pathological change in many lung diseases, its occurrence and development are controlled by a variety of cells, cytokines and proteases. Studies have shown that autophagy plays an important role in the processes of pulmonary inflammation and fibrosis, which can alleviate pulmonary fibrosis by inhibiting the secretion of inflammatory cytokines and fibroblast-promoting factors, degrading the collagen in fibroblasts and inhibiting the process of epithelial-mesenchymal transition (EMT). This paper, will give a brief summary on the role and mechanism of autophagy in idiopathic pulmonary fibrosis (IPF), pulmonary cystic fibrosis (PCF) and silicosis pulmonary fibrosis thereby provide some reference for future work.