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.

中文翻译：

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肺纤维化发病机制的新见解：纤维化发作时的 RBM7–NEAT1–CXCL12–SatM 轴

纤维化是一种危及生命的疾病，具有显着的发病率和死亡率，是由可影响几个重要器官的结缔组织过度形成引起的。器官组织中的纤维化是由反复损伤造成的异常伤口愈合过程引起的。在我们最近使用博莱霉素诱导的肺纤维化小鼠模型的研究中，我们检查了 RNA 结合蛋白 7 (RBM7) 在肺纤维化发展中的作用。RBM7 在受损的肺上皮细胞中上调，并通过促进受损上皮细胞的凋亡来干扰正常的上皮细胞修复和再生。RBM7 导致富含核的丰富转录物 1 (NEAT1) 的衰变，从而导致肺上皮细胞的凋亡。然后这些凋亡细胞产生 C-X-C 基序趋化因子配体 12 (CXCL12)，这导致将称为分离核的非典型单核细胞（SatM）的促进纤维化的单核细胞群募集到受损区域，然后引发和促进肺纤维化。在这里，我们回顾了最近对肺纤维化发展过程中肺实质细胞和造血细胞之间串扰的见解。