PMID- 34165514
OWN - NLM
STAT- MEDLINE
DCOM- 20220322
LR  - 20220322
IS  - 1460-2377 (Electronic)
IS  - 0953-8178 (Linking)
VI  - 33
IP  - 12
DP  - 2021 Nov 25
TI  - Novel insights into the pathogenesis of lung fibrosis: the RBM7-NEAT1-CXCL12-SatM 
      axis at fibrosis onset.
PG  - 659-663
LID - 10.1093/intimm/dxab034 [doi]
AB  - 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 
      motif protein 7 (RBM7) on the development of lung fibrosis. RBM7 is up-regulated 
      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 cross-talk 
      between lung parenchymal cells and hematopoietic cells during the development of 
      pulmonary fibrosis.
CI  - (c) The Japanese Society for Immunology. 2021. All rights reserved. For 
      permissions, please e-mail: journals.permissions@oup.com.
FAU - Fukushima, Kiyoharu
AU  - Fukushima K
AD  - Department of Host Defense, Research Institute for Microbial Diseases (RIMD), 
      Osaka University, Osaka, Japan.
AD  - Laboratory of Host Defense, World Premier Institute-Immunology Frontier Research 
      Center (WPI-IFReC), Osaka University, Osaka, Japan.
AD  - Department of Respiratory Medicine and Clinical Immunology, Graduate School of 
      Medicine, Osaka University, Osaka, Japan.
FAU - Akira, Shizuo
AU  - Akira S
AD  - Department of Host Defense, Research Institute for Microbial Diseases (RIMD), 
      Osaka University, Osaka, Japan.
AD  - Laboratory of Host Defense, World Premier Institute-Immunology Frontier Research 
      Center (WPI-IFReC), Osaka University, Osaka, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - England
TA  - Int Immunol
JT  - International immunology
JID - 8916182
RN  - 0 (CXCL12 protein, human)
RN  - 0 (Chemokine CXCL12)
RN  - 0 (NEAT1 long non-coding RNA, human)
RN  - 0 (RBM7 protein, human)
RN  - 0 (RNA, Long Noncoding)
RN  - 0 (RNA-Binding Proteins)
SB  - IM
MH  - Chemokine CXCL12/*immunology
MH  - Humans
MH  - Monocytes/*immunology
MH  - Pulmonary Fibrosis/*immunology/pathology
MH  - RNA, Long Noncoding/*immunology
MH  - RNA-Binding Proteins/*immunology
OTO - NOTNLM
OT  - RNA decay
OT  - macrophage
OT  - ncRNA
EDAT- 2021/06/25 06:00
MHDA- 2022/03/23 06:00
CRDT- 2021/06/24 12:24
PHST- 2021/05/28 00:00 [received]
PHST- 2021/08/04 00:00 [accepted]
PHST- 2021/06/25 06:00 [pubmed]
PHST- 2022/03/23 06:00 [medline]
PHST- 2021/06/24 12:24 [entrez]
AID - 6308740 [pii]
AID - 10.1093/intimm/dxab034 [doi]
PST - ppublish
SO  - Int Immunol. 2021 Nov 25;33(12):659-663. doi: 10.1093/intimm/dxab034.