Emphysema, as one of the main clinicopathological symptoms of chronic obstructive pulmonary disease (COPD), features unclear pathogenesis, prolonged course and complex lesion types, and so far there are still no effective targeted therapeutic drugs for it.
Prof. Hu Xuefeng and Prof. Zhang Yanding’s research team of College of Life Sciences found in human emphysema samples that downregulated BMP-Smad1/5/8 signaling may be a potential pathogenesis of emphysema. The team successfully mimicked the typical pathological features of human emphysema by downregulating BMP-Smad1/5/8 signaling in mouse lungs. Further analysis showed that dysregulation of BMP-Smad1/5/8 signaling reduced the secretory and metabolic functions of alveolar type II epithelial cells (AT2s) and inhibited AT2 proliferation and differentiation, resulting in inflammatory destruction and ineffective damage repair of the lungs, and thus leading to emphysema. Reactivation of BMP-Smad1/5/8 signaling by genetics or chemotherapy significantly attenuated the morphology and pathophysiology of emphysema and improved the lung function in the mouse model. The team also found that BMP-Smad1/5/8 signaling is located at the top of the signaling cascade that regulates lung homeostasis, and that its dysregulation is a key factor causing emphysema. The study sheds new light on the pathogenesis of emphysema, and suggests that BMP-Smad1/5/8 signaling could serve as a potential target for future prevention and treatment of pulmonary emphysema.
The research findings, titled “Downregulated BMP–Smad1/5/8 signaling causes emphysema via dysfunction of alveolar type II epithelial cells,” have recently been published in Journal of Pathology, a top international academic journal in the field of pathology. FNU is the only affiliation of the paper, with Prof. Hu Xuefeng and Prof. Zhang Yanding as the corresponding authors, Zheng Xi, a postdoctoral student of FNU, as the first author, and Prof. Chen Yiping of Tulane University (USA) and Prof. Lai Fancai of the First Affiliated Hospital of Fujian Medical University as the co-authors. The research was funded by the National Natural Science Foundation of China.
Paper link：https://pathsocjournals.onlinelibrary.wiley.com/doi/10.1002/path.6234
(Translated by Zou Chenxin/ Reviewed by Xie Xiujuan)