Evidence map›Paper›PMID 36227848›Full record

ArticleAmerican journal of respiratory cell and molecular biology2023

Adenovirus-mediated Overexpression of FcγRIIB Attenuates Pulmonary Inflammation and Fibrosis.

Zhe Zhang, Zhujie Cao, Lin Hou, Meiyue Song, Yitian Zhou, Yiling Chen, Huiyuan Hu, Yangfeng Hou, Ying Liu, Bolun Li and 13 more

Abstract read
PubMed Publisher
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. Gene Therapy for Occupational Lung Disease: Steering Macrophages in the Right Direction?American journal of respiratory cell and molecular biology · 2023
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

23 authors at 4 institutions in 1 country.

Zhe ZhangDepartment of Pulmonary and Critical Care Medicine, The First Hospital of Shanxi Medical University, Taiyuan, China.
Zhujie CaoDepartment of Physiology and.
Lin HouDepartment of Physiology and.
Meiyue SongDepartment of Physiology and.
Yitian ZhouDepartment of Pathophysiology, State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Yiling ChenDepartment of Physiology and.
Huiyuan HuDepartment of Physiology and.
Yangfeng HouDepartment of Pathophysiology, State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Ying LiuDepartment of Physiology and.
Bolun LiDepartment of Physiology and.
Xiaomin SongDepartment of Pathophysiology, State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Weipeng GeDepartment of Pathophysiology, State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Baicun LiDepartment of Physiology and.
Xuehan JiangDepartment of Physiology and.
Jie YangDepartment of Physiology and.
Dingyun SongDepartment of Pulmonary and Critical Care Medicine, Center of Respiratory Medicine, China-Japan Friendship Hospital, Beijing, China.
Xinri ZhangDepartment of Pulmonary and Critical Care Medicine, The First Hospital of Shanxi Medical University, Taiyuan, China.
Junling PangDepartment of Physiology and.
Tiantian ZhangDepartment of Physiology and.
Hong ZhangDepartment of Physiology and.
Peiran YangDepartment of Physiology and.ORCID 0000-0002-4635-1215
Jing WangDepartment of Pulmonary and Critical Care Medicine, The First Hospital of Shanxi Medical University, Taiyuan, China.
Chen WangDepartment of Pulmonary and Critical Care Medicine, The First Hospital of Shanxi Medical University, Taiyuan, China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNShanxi Medical University · CNFirst Affiliated Hospital of Xi'an Jiaotong University · CNChina-Japan Friendship Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Progressive fibrosing interstitial lung diseases (PF-ILDs) result in high mortality and lack effective therapies. The pathogenesis of PF-ILDs involves macrophages driving inflammation and irreversible fibrosis. Fc-γ receptors (FcγRs) regulate macrophages and inflammation, but their roles in PF-ILDs remain unclear. We characterized the expression of FcγRs and found upregulated FcγRIIB in human and mouse lungs after exposure to silica. FcγRIIB deficiency aggravated lung dysfunction, inflammation, and fibrosis in silica-exposed mice. Using single-cell transcriptomics and

Indexed as

Lung Diseases, InterstitialPneumoniaAdenoviridaeAnimalsFibrosisHumansInflammationMiceReceptors, IgGSilicon DioxideReceptors, IgGSilicon DioxideFcγRIIBmacrophagespulmonary fibrosispulmonary functionSpp1

Identifiers

PMID36227848
OpenAlexW4305057585

What OpenQuestion holds

Textmetadata
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.