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Role of c-Jun N-Terminal Kinase in Radiation-Induced Lung Fibrosis*

Soo-taek Uh, MD; Do Jin Kim, MD; Seung Hyuk Moon, MD; Yong Hoon Kim, MD; Uk Seok Kim, MD; Doo Ho Choi, MD; Choon Sik Park, MD
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*From the Departments of Internal Medicine (Drs. Uh, D.J. Kim, Moon, Y.H. Kim, and Park) and Radiation Oncology (Drs. U.S. Kim and Choi), Soon Chun Hyang University Hospital, Seoul, Korea.

Correspondence to: S. Uh, MD, Department of Internal Medicine, Soon Chun Hyang University Hospital, 657–58 Hannam-Dong, Yongsan-Ku, Seoul, 140-743, Korea



Chest. 2001;120(1_suppl):S63-S64. doi:10.1378/chest.120.1_suppl.S63
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The underlying pathogenesis of radiation-induced lung fibrosis (RTLF) has not been defined very well. However, the role of transforming growth factor (TGF)-β has been focused on the generation of RTLF because of its increased expression in irradiation-induced fibrotic lung lesions,1 and TGF-β messenger RNA and protein preceded RTLF.2 The downstream signal after TGF-β stimulation-resulting lung fibrosis includes the activation of a lot of mediators, like Smad and c-Jun N-terminal kinase (JNK) through TAK1.3 We hypothesized that the activation of JNK may have a pivotal role in the pathogenesis of RTLF through the increased transcription of fibrogenic cytokines. The present study evaluates the activity of JNK in alveolar macrophages after radiation, and the relationship with the activity of JNK and the amount of collagen in lung tissues.

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