The work is to investigate expressions and roles of Smad3, Smad4 and Smad7 in pathogenesis of pulmonary fibrosis of rats. Altogether 60 specific-pathogen-free Wistar rats were used in the study, with 50 of them being irradiated with 25Gy ,60,Co γ−rays on whole thoracic region. The rats were sacrificed and specimens were harvested in 1 day, 1 week, 1month and 3 months after the irradiation. Alveolar macrophages were obtained and cultured. Expressions of Smad3, Smad4 and Smad7 were observed by immunohistochemistry. In normal pulmonary tissue, expressions of Smad3, Smad4 and Smad7 could be seen in the plasma of endothelial cells and smooth muscle cells of blood vessel. Expressions of Smad4 could be seen in the plasma of epithelial cells of bronchi. One day after the irradiation, expressions of the three proteins could be seen in the plasma of some pneumocytes and macrophages. One week and even one month after the irradiation, expressions of Smad4 could be seen in the plasma of some fibroblasts. Three months after the irradiation, expressions of Smad4 could be seen in the nucleus of endothelial cells, macrophages and fibroblasts. The cells, in which Smad3, Smad4 and Smad7 are positive, are main target or effect cells related to the initiation and development of radiation pneumonia and fibrosis. This indicates that Smad signaling might be a key pathway of TGF β−mediated radiation pulmonary injury.