Evidence map›Paper›PMID 33012781›Full record

ArticleCell death & disease2020

Small GTPase RAB6 deficiency promotes alveolar progenitor cell renewal and attenuates PM2.5-induced lung injury and fibrosis.

Lawei Yang, Gang Liu, Xiaomin Li, Zhengyuan Xia, Yahong Wang, Weihao Lin, Wei Zhang, Wenjuan Zhang, Xuenong Li

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 2 pooled it
4.6field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 2 syntheses or guidelines pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. The impact of particulate matter 2.5 on the risk of hepatocellular carcinoma: a meta-analysis.International archives of occupational and environmental health · 2022
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  19. A comparative study on the model of PMEnvironmental science and pollution research international · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 2 countries.

Lawei Yang *Department of Pathology, School of Basic Medical Sciences, Southern Medical University, 510515, Guangzhou, China.
Gang Liu *Clinical Research Center, Affiliated Hospital of Guangdong Medical University, 524001, Zhanjiang, China.
Xiaomin Li *Department of Pathology, School of Basic Medical Sciences, Southern Medical University, 510515, Guangzhou, China.
Zhengyuan XiaClinical Research Center, Affiliated Hospital of Guangdong Medical University, 524001, Zhanjiang, China.ORCID http://orcid.org/0000-0001-6844-5928
Yahong WangClinical Research Center, Affiliated Hospital of Guangdong Medical University, 524001, Zhanjiang, China.
Weihao LinDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, 510515, Guangzhou, China.
Wei ZhangDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, 510515, Guangzhou, China.
Wenjuan ZhangDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, 510515, Guangzhou, China.
Xuenong LiDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, 510515, Guangzhou, China. doctor_lixuenong@126.com.
Southern Medical University · CNGuangdong Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease characterized by chronic non-specific inflammation of the interstitial lung and extensive deposition of collagen fibers leading to destruction of lung function. Studies have demonstrated that exposure to fine particulate matter (PM2.5) increases the risk of IPF. In order to recover from PM2.5-induced lung injury, alveolar epithelial cells need to be repaired and regenerated to maintain lung function. Type 2 alveolar epithelial cells (AEC2) are stem cells in the adult lung that contribute to the lung repair process through complex signaling. Our previous studies demonstrated that RAB6, a RAS family member lowly expressed in lung cancer, inhibited lung cancer stem cell self-renewal, but it is unclear whether or not and how RAB6 may regulate AEC2 cell proliferation and self-renewal in PM2.5-induced pulmonary fibrosis. Here, we demonstrated that knockout of RAB6 inhibited pulmonary fibrosis, oxidative stress, and AEC2 cell death in PM2.5-injured mice. In addition, knockout of RAB6 decreased Dickkopf 1(DKK1) autocrine and activated proliferation, self-renewal, and wnt/β-catenin signaling of PM2.5-injured AEC2 cells. RAB6 overexpression increased DKK1 autocrine and inhibited proliferation, self-renewal and wnt/β-catenin signaling in AEC2 cells in vitro. Furthermore, DKK1 inhibitors promoted proliferation, self-renewal and wnt/β-catenin signaling of RAB6 overexpressing AEC2 cells, and attenuated PM2.5-induced pulmonary fibrosis in mice. These data establish RAB6 as a regulator of DKK1 autocrine and wnt/β-catenin signal that serves to regulate AEC2 cell proliferation and self-renewal, and suggest a mechanism that RAB6 disruption may promote AEC2 cell proliferation and self-renewal to enhance lung repair following PM2.5 injury.

Indexed as

AnimalsCell ProliferationCell Self RenewalFibrosisHumansIdiopathic Pulmonary FibrosisLungLung InjuryMice, Inbred C57BLParticulate Matterrab GTP-Binding ProteinsStem CellsWnt Signaling PathwayParticulate MatterRab6 proteinrab GTP-Binding Proteins

Identifiers

PMID33012781
PMCPMC7533251
OpenAlexW3091342448

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.