Laboratory of Mucosal Immunology and Immunoregulation, VIB Center for Inflammation Research, Ghent, Belgium; Department of Internal Medicine and Pediatrics, Ghent University, Ghent, Belgium.
Laboratory of Mucosal Immunology and Immunoregulation, VIB Center for Inflammation Research, Ghent, Belgium; Department of Internal Medicine and Pediatrics, Ghent University, Ghent, Belgium; Department of Pulmonary Medicine, Erasmus Medical Center, Rotterdam, the Netherlands.
Immunity. 2020 Mar 17;52(3):429-431. doi: 10.1016/j.immuni.2020.02.008.
The initial molecular events and the cell type(s) responsible for the development of fibrosis are unclear. Fukushima, Satoh, et al. find that increased expression of the nuclear exosome targeting complex component Rbm7 in lung epithelial cells promotes the degradation of the long non-coding RNA NEAT1, impairs DNA repair, and triggers apoptosis. Dying epithelial cells release chemokines that recruit atypical monocytes, which drive tissue fibrosis.
纤维化发生的初始分子事件和（或）细胞类型尚不清楚。Fukushima、Satoh 等人发现，肺上皮细胞中核外切体靶向复合物成分 Rbm7 的表达增加，促进了长链非编码 RNA NEAT1 的降解，损害了 DNA 修复，并引发细胞凋亡。死亡的上皮细胞释放趋化因子招募非典型单核细胞，进而导致组织纤维化。
