Evidence map›Paper›PMID 31341890›Full record

ReviewBioMed research international2019

Cigarette Smoke Induced Lung Barrier Dysfunction, EMT, and Tissue Remodeling: A Possible Link between COPD and Lung Cancer.

Wei Hou, Siyi Hu, Chunyan Li, Hanbin Ma, Qi Wang, Guangping Meng, Tingting Guo, Jie Zhang

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in BioMed research international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed, 1 pooled it
12.9field-weighted citation impact, top 1% 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

93 citing papers in PubMed, 1 synthesis or guideline pooled it, 164 citations in OpenAlex.

  1. Pooled it
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  7. The role and mechanisms of the HIF-1 signaling pathway in LC-COPD.Journal of cancer research and clinical oncology · 2025
    Review
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33 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 1 country.

Wei HouDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Jilin University, Changchun 130041, China.
Siyi HuCAS Key Laboratory of Bio-Medical Diagnostics, Suzhou Institute of Biomedical Engineering and Technology, Chinese Academy of Science, Suzhou 215163, China.
Chunyan LiDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Jilin University, Changchun 130041, China.
Hanbin MaCAS Key Laboratory of Bio-Medical Diagnostics, Suzhou Institute of Biomedical Engineering and Technology, Chinese Academy of Science, Suzhou 215163, China.
Qi WangDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Jilin University, Changchun 130041, China.
Guangping MengDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Jilin University, Changchun 130041, China.
Tingting GuoDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Jilin University, Changchun 130041, China.
Jie ZhangDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Jilin University, Changchun 130041, China.ORCID https://orcid.org/0000-0001-6795-8000
Second Affiliated Hospital of Jilin University · CNSuzhou Institute of Biomedical Engineering and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) and lung cancer, closely related to smoking, are major lung diseases affecting millions of individuals worldwide. The generated gas mixture of smoking is proved to contain about 4,500 components such as carbon monoxide, nicotine, oxidants, fine particulate matter, and aldehydes. These components were considered to be the principle factor driving the pathogenesis and progression of pulmonary disease. A large proportion of lung cancer patients showed a history of COPD, which demonstrated that there might be a close relationship between COPD and lung cancer. In the early stages of smoking, lung barrier provoked protective response and DNA repair are likely to suppress these changes to a certain extent. In the presence of long-term smoking exposure, these mechanisms seem to be malfunctioned and lead to disease progression. The infiltration of inflammatory cells to mucosa, submucosa, and glandular tissue caused by inhaled cigarette smoke is responsible for the destruction of matrix, blood supply shortage, and epithelial cell death. Conversely, cancer cells have the capacity to modulate the proliferation of epithelial cells and produce of new vascular networks. Comprehension understanding of mechanisms responsible for both pathologies is necessary for the prevention and treatment of COPD and lung cancer. In this review, we will summarize related articles and give a glance of possible mechanism between cigarette smoking induced COPD and lung cancer.

Indexed as

Airway RemodelingBlood-Air BarrierCigarette SmokingExtracellular MatrixLung NeoplasmsPulmonary Disease, Chronic ObstructiveHumansTime Factors

Identifiers

PMID31341890
PMCPMC6613007
OpenAlexW2951663586

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.