Shencun Fang, Huifang Guo, Yusi Cheng, Zewei Zhou et al.
Abstract Excessive proliferation and migration of fibroblasts contribute to pulmonary fibrosis in silicosis, and both epithelial cells and endothelial cells participate in the accumulation of fibroblasts via the epithelial–mesenchymal transition (EMT) and the endothelial–mesenchymal transition (EndM...
Haijun Liu, Shencun Fang, Wei Wang, Yusi Cheng et al.
Silicosis is characterized by accumulation of fibroblasts and excessive deposition of extracellular matrix. Monocyte chemotactic protein-1-induced protein 1 (MCPIP1) plays a critical role in fibrosis induced by SiO2. However, the details of the downstream events of MCPIP1 activity in pulmonary fibro...
Xueting Liu, Shencun Fang, Haijun Liu, Xingang Wang et al.
Background Silicosis is a systemic disease caused by inhaling silicon dioxide (SiO2). Phagocytosis of SiO2 in the lung initiates an inflammatory cascade that results in fibroblast proliferation and migration and subsequent fibrosis. Clinical evidence indicates that the activation of alveolar macroph...
Juan Yin, Jing Wang, Xinxin Zhang, Yan Liao et al.
Abstract Background Pulmonary fibrosis initiates a pneumonic cascade that leads to fibroblast dysfunction characterized by excess proliferation. Anoikis is a physiological process that ensures tissue development and homeostasis. Researchers have not clearly determined whether disruption of anoikis i...