Evidence map›Paper›PMID 38029327›Full record

ArticleAmerican journal of respiratory cell and molecular biology2024

GOLM1 Promotes Pulmonary Fibrosis through Upregulation of

Yani Wang, Danjing Hu, Linyan Wan, Shuhui Yang, Song Liu, Zixi Wang, Jie Li, Jia Li, Zhoude Zheng, Chongsheng Cheng and 10 more

Abstract read
PubMed Publisher
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Observational
  3. Article
  4. AAmerican journal of respiratory cell and molecular biology · 2024
    Article
  5. Review
4 · The record

Corrections and comments

  • Commented on by
    A2024
5 · Who and what money

Authors and funding

20 authors at 4 institutions in 1 country.

Yani WangDepartment of Pulmonary and Critical Care Medicine and.
Danjing HuDepartment of Pulmonary and Critical Care Medicine and.
Linyan WanState Key Laboratory of Common Mechanism Research for Major Diseases, Haihe Laboratory of Cell Ecosystem, Department of Physiology, Institutes of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Shuhui YangState Key Laboratory of Common Mechanism Research for Major Diseases, Haihe Laboratory of Cell Ecosystem, Department of Physiology, Institutes of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Song LiuMedical Science Center, State Key Laboratory of Complex, Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Zixi WangDepartment of Biochemistry & Molecular Biology, School of Basic Medicine, Anhui Medical University, Hefei, China.
Jie LiState Key Laboratory of Common Mechanism Research for Major Diseases, Haihe Laboratory of Cell Ecosystem, Department of Physiology, Institutes of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Jia LiDepartment of Pulmonary and Critical Care Medicine and.
Zhoude ZhengDepartment of Pulmonary and Critical Care Medicine and.
Chongsheng ChengDepartment of Pulmonary and Critical Care Medicine and.
Yanan WangState Key Laboratory of Common Mechanism Research for Major Diseases, Haihe Laboratory of Cell Ecosystem, Department of Physiology, Institutes of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Hanghang WangDepartment of Pulmonary and Critical Care Medicine and.
Xinlun TianDepartment of Pulmonary and Critical Care Medicine and.
Wenhui ChenDepartment of Lung Transplantation, Centre for Lung Transplantation, Centre for Respiratory Diseases, China-Japan Friendship Hospital, Beijing, China.
Shanqing LiDepartment of Thoracic Surgery, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China; and.
Ji ZhangLung Transplantation Center, Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi, China.
Xiaojun ZhaDepartment of Biochemistry & Molecular Biology, School of Basic Medicine, Anhui Medical University, Hefei, China.
Jingyu ChenLung Transplantation Center, Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi, China.
Hongbing ZhangState Key Laboratory of Common Mechanism Research for Major Diseases, Haihe Laboratory of Cell Ecosystem, Department of Physiology, Institutes of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0000-0001-6291-1027
Kai-Feng XuDepartment of Pulmonary and Critical Care Medicine and.ORCID 0000-0002-7662-531X
Chinese Academy of Medical Sciences & Peking Union Medical College · CNAnhui Medical University · CNWuxi People's Hospital · CNChina-Japan Friendship Hospital · CN

Funding

Chinese Academy of Medical Sciences (CAMS) Innovation Fund for Medical Sciences CIFMS 2021-I2M-1-003National Key Research and Development Program of China 2021YFC2500700National Natural Science Foundation of China 82170084National Natural Science Foundation of China U20A20341PUMCH High Quality Clinical Research Project 2022-PUMCH-B-107
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a lethal progressive disease with elusive molecular mechanisms and limited therapeutic options. Aberrant activation of fibroblasts is a central hallmark of lung fibrosis. Here, we report that Golgi membrane protein 1 (GOLM1, also known as GP73 or GOLPH2) was increased in the lungs of patients with pulmonary fibrosis and mice with bleomycin (BLM)-induced pulmonary fibrosis. Loss of GOLM1 inhibited proliferation, differentiation, and extracellular matrix deposition of fibroblasts, whereas overexpression of GOLM1 exerted the opposite effects. Similarly, worsening pulmonary fibrosis after BLM treatment was observed in

Indexed as

Idiopathic Pulmonary FibrosisAnimalsBleomycinExtracellular MatrixFibroblastsHumansMembrane ProteinsMiceMice, KnockoutPhosphoproteinsUp-RegulationBleomycinGOLM1 protein, humanGolm1 protein, mouseMembrane ProteinsPhosphoproteinsGolgi membrane protein 1GP73KLF4NEAT1pulmonary fibrosis

Identifiers

PMID38029327
OpenAlexW4389122534

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.