• Bruno Crestani, Sylvain Marchand-Adam, Christophe Quesnel, Laurent Plantier, Keren Borensztajn, Joelle Marchal, Arnaud Mailleux, Paul Soler, and Monique Dehoux.
• Service de Pneumologie A, Hôpital Bichat, 46 rue Henri Huchard, Paris CEDEX 18, France. bruno.crestani@bch.aphp.fr
• Proc Am Thorac Soc. 2012 Jul 1;9(3):158-63.

AbstractIdiopathic 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.

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