当前位置: X-MOL 学术Immunity › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Rbm7 in Structural Cells: A NEAT Way to Control Fibrosis.
Immunity ( IF 25.5 ) Pub Date : 2020-03-17 , DOI: 10.1016/j.immuni.2020.02.008
Hamida Hammad 1 , Bart N Lambrecht 2
Affiliation  

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.



中文翻译:

结构细胞中的Rbm7:一种控制纤维化的有效方法。

尚不清楚引起纤维化发展的最初分子事件和细胞类型。福岛,佐藤等。发现在肺上皮细胞中靶向核复合体Rbm7的核外泌体表达的增加促进了长的非编码RNA NEAT1的降解,削弱了DNA修复,并触发了细胞凋亡。垂死的上皮细胞释放趋化因子,这些趋化因子募集非典型单核细胞,从而驱动组织纤维化。

更新日期:2020-03-19
down
wechat
bug