Evidence map›Paper›PMID 32158205›Full record

ArticleInternational journal of chronic obstructive pulmonary disease2020

Serum Endostatin Is a Novel Marker for COPD Associated with Lower Lung Function, Exacerbation and Systemic Inflammation.

Yanqiu Wu, Jiangyue Qin, Junyun He, Yongchun Shen, Hao Wang, Yanping Li, Qianglin Zeng, Jiajia Dong, Yunfei An, Shuguang Xiong and 2 more

Open access · goldAbstract read
In one paragraph

Article in International journal of chronic obstructive pulmonary disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. [MBD1 knockdown inhibits proliferation, migration and angiogenesis of human umbilical vein endothelial cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
    Article
  2. Basement membranes in lung development, disease, and repair.Matrix biology : journal of the International Society for Matrix Biology · 2025
    Review
  3. Article
  4. Article
  5. Review
  6. Cross-platform proteomics signatures of extreme old age.bioRxiv : the preprint server for biology · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Caudamins, a new subclass of protein hormones.Trends in endocrinology and metabolism: TEM · 2021
    Review
  12. Observational
  13. Review
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

12 authors at 4 institutions in 1 country.

Yanqiu WuDivision of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China.
Jiangyue QinDivision of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China.
Junyun HeDepartment of Respiratory and Critical Care Medicine, Hospital of Chengdu Office of People's Government of Tibetan Autonomous Region, Chengdu, Sichuan, People's Republic of China.
Yongchun ShenDivision of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China.
Hao WangDivision of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China.
Yanping LiDepartment of Respiratory and Critical Care Medicine, Third People's Hospital of Chengdu, Sichuan, People's Republic of China.
Qianglin ZengDepartment of Respiratory and Critical Care Medicine, Affiliated Hospital of Chengdu University, Chengdu, Sichuan, People's Republic of China.
Jiajia DongDivision of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China.
Yunfei AnDepartment of Laboratory Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China.
Shuguang XiongDepartment of Respiratory and Critical Care Medicine, 416 Hospital of Nuclear Industry, Chengdu, Sichuan, People's Republic of China.
Mei FengDepartment of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China.
Fuqiang WenDivision of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China.ORCID 0000-0001-6205-4758
Sichuan University · CNChengdu University · CNThird People's Hospital of Chengdu · CNTibet Autonomous Region People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Backgrounds and Aims: It is well known that angiogenesis contributes to the progression of chronic obstructive pulmonary disease (COPD) by initiating the remodeling of bronchial vasculature. However, the specific molecular mechanisms are incompletely understood. This research aimed to explore whether endostatin, a member of endogenous antiangiogenic proteins, is a biomarker in COPD and plays a role in the angiogenesis of COPD. Methods: 100 stable COPD patients, 130 patients with acute exacerbation (AECOPD) and 68 healthy volunteers were recruited in this research. Lung function test was conducted in the healthy people and stable COPD patients. Serum endostatin, C-reactive protein (CRP) and vascular endothelial growth factor (VEGF) of all the subjects were measured by Human Magnetic Luminex Screening Assay. Results: Serum endostatin level was significantly higher in stable COPD compared with healthy control and even more in AECOPD patients (P<0.001). Besides, stable COPD patients with frequent exacerbation (≥2 exacerbations per year) in the last 1 year had a higher concentration of endostatin in the circulation compared to the patients with less exacerbation (P=0.037). Furthermore, circulatory endostatin was negatively associated with forced expiratory volume in 1 s % predicted (FEV Conclusion: These results suggested that endostatin is a biomarker for COPD and associated with lower lung function, exacerbation, and systemic inflammation. Endostatin potentially contributes to the pathogenesis of COPD.

Indexed as

AdultAgedBiomarkersCollagen Type VIIICollagen Type XVIIIC-Reactive ProteinCross-Sectional StudiesDisease ProgressionEndostatinsFemaleForced Expiratory VolumeHumansInflammation MediatorsLungMaleMiddle AgedBiomarkersCOL18A1 protein, humanCollagen Type VIIICollagen Type XVIIIC-Reactive ProteinEndostatinsInflammation MediatorsVascular Endothelial Growth Factor AVEGFA protein, humanangiogenesischronic obstructive pulmonary diseaseendostatininflammationlung function

Identifiers

PMID32158205
PMCPMC7049271
OpenAlexW3007399857

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.