Overexpression of Pulmonary Surfactant Protein B in Alveolar Type II Epithelial Cells and Its Potential Role in Idiopathic Pulmonary Fibrosis

ZHENG Xi^1,2, WANG Linfang¹, WANG Guoyan¹, WANG Shaobing², LIU Yiping², HU Xuefeng^1*

(¹Fujian Key Laboratory of Developmental and Neural Biology, College of Life Sciences, Fujian Normal University, Fuzhou 350117, China; ²Provincial University Key Laboratory of Sport and Health Science, School of Physical Education and Sport Sciences, Fujian Normal University, Fuzhou 350117, China)

Abstract:

IPF (idiopathic pulmonary fibrosis) is a severe chronic lung disease with complex etiology and lacking effective treatment. This study aimed to investigate the function and mechanism of pulmonary SP-B (sur factant protein B) in IPF by constructing a transgenic mouse model that specifically overexpressed SP-B in alveolar type II epithelial cells. The overexpression of SP-B led to structural damage in lung tissue, abnormal extracellular matrix deposition, and pulmonary inflammation, highlighting its critical role in IPF pathogenesis. Furthermore, SP-B promoted pulmonary fibrosis by regulating the TGF-β signaling pathway to affect cell proliferation and ex tracellular matrix protein expression. These findings offer new insights into the etiology of IPF and potential targets for Sftpb gene-based therapeutic strategies.

CSTR: 32200.14.cjcb.2024.10.0005