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Novel insights into the pathogenesis of lung fibrosis: the RBM7-NEAT1-CXCL12-SatM axis at fibrosis onset.

Fibrosis is a life-threatening disorder with significant morbidity and mortality and is caused by excessive formation of connective tissue that can affect several important organs. Fibrosis in organ tissues is caused by an abnormal wound-healing process from repeated injuries. In our recent study using a mouse model of bleomycin-induced lung fibrosis, we examined the role of RNA-binding protein 7 (RBM7) on the development of lung fibrosis. RBM7 is upregulated in the injured lung epithelium and disturbs normal epithelial cell repair and regeneration by promoting apoptosis of damaged epithelial cells. RBM7 causes the decay of nuclear-enriched abundant transcript 1 (NEAT1), which results in apoptosis of lung epithelial cells. These apoptotic cells then produce C-X-C motif chemokine ligand 12 (CXCL12), which leads to the recruitment of a fibrosis-promoting monocyte population called segregated-nucleus-containing atypical monocytes (SatM) to the damaged area, followed by the initiation and promotion of lung fibrosis. Here, we review recent insights into the crosstalk between lung parenchymal cells and hematopoietic cells during the development of pulmonary fibrosis.