2020-03-17
Rbm7 in Structural Cells: A NEAT Way to Control Fibrosis
Publication
Publication
Immunity , Volume 52 - Issue 3 p. 429- 431
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.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.
Additional Metadata | |
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doi.org/10.1016/j.immuni.2020.02.008, hdl.handle.net/1765/125501 | |
Immunity | |
Organisation | Department of Pulmonology |
Hammad, H., & Lambrecht, B. (2020). Rbm7 in Structural Cells: A NEAT Way to Control Fibrosis. Immunity, 52(3), 429–431. doi:10.1016/j.immuni.2020.02.008 |