A potential role of the JNK pathway in hyperoxia-induced cell death myofibroblast transdifferentiation and TGF-β1-mediated injury in the developing murine lung

摘要

BackgroundTransforming growth factor-beta 1 (TGF-β1) has been implicated in hyperoxia-induced cell death and impaired alveolarization in the developing lung. In addition, the c-JunNH2-terminal kinase (JNK) pathway has been shown to have a role for TGF-β1-mediated effects. We hypothesized that the JNK pathway is an important regulator of hyperoxia-induced pulmonary responses in the developing murine lung.