Service de Pneumologie A, Hôpital Bichat, 46 rue Henri Huchard, Paris CEDEX 18, France.
Proc Am Thorac Soc. 2012 Jul;9(3):158-63. doi: 10.1513/pats.201202-018AW.
Idiopathic pulmonary fibrosis is currently believed to be driven by alveolar epithelial cells, with abnormally activated alveolar epithelial cells accumulating in an attempt to repair injured alveolar epithelium (1). Thus, targeting the alveolar epithelium to prevent or inhibit the development of pulmonary fibrosis might be an interesting therapeutic option in this disease. Hepatocyte growth factor (HGF) is a growth factor for epithelial and endothelial cells, which is secreted by different cell types, especially fibroblasts and neutrophils. HGF has mitogenic, motogenic, and morphogenic properties and exerts an antiapoptotic action on epithelial and endothelial cells. HGF has also proangiogenic effect. In vitro, HGF inhibits epithelial-to-mesenchymal cell transition and promotes myofibroblast apoptosis. In vivo, HGF has antifibrotic properties demonstrated in experimental models of lung, kidney, heart, skin, and liver fibrosis. Hence, the modulation of HGF may be an attractive target for the treatment of lung fibrosis.
特发性肺纤维化目前被认为是由肺泡上皮细胞驱动的，异常激活的肺泡上皮细胞聚集在试图修复受损的肺泡上皮细胞(1)。因此，针对肺泡上皮细胞，以防止或抑制肺纤维化的发展，可能是这种疾病的一个有趣的治疗选择。肝细胞生长因子(HGF)是上皮细胞和内皮细胞的生长因子，由不同的细胞类型分泌，特别是成纤维细胞和中性粒细胞。HGF 具有有丝分裂、趋化性和形态发生特性，并对上皮细胞和内皮细胞发挥抗凋亡作用。HGF 还具有促血管生成作用。在体外，HGF 抑制上皮细胞向间充质细胞转化，促进肌成纤维细胞凋亡。在体内，HGF 在肺、肾、心、皮肤和肝纤维化的实验模型中具有抗纤维化特性。因此，HGF 的调节可能是治疗肺纤维化的一个有吸引力的靶点。
