Evidence map›Paper›PMID 31557398›Full record

ArticleJournal of cellular and molecular medicine2019

Long non-coding RNA TUG1 promotes airway remodelling by suppressing the miR-145-5p/DUSP6 axis in cigarette smoke-induced COPD.

Wenchao Gu, Yaping Yuan, Linxuan Wang, Hua Yang, Shanshan Li, Zhijun Tang, Qiang Li

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.

  1. Pooled it
  2. Review
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  4. Review
  5. Exploring the Roles of Wnt Signaling Pathway and Non-Coding RNAs in COPD.International journal of chronic obstructive pulmonary disease · 2026
    Review
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  7. Article
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  10. Article
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  13. Article
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  18. The role ofHeliyon · 2023
    Article
  19. Article
  20. Roles of noncoding RNAs in chronic obstructive pulmonary disease.Journal of translational internal medicine · 2023
    Article
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

7 authors at 2 institutions in 1 country.

Wenchao GuDepartment of Respiratory Medicine, Changhai Hospital, Second Military Medical University, Shanghai, China.
Yaping YuanDepartment of Respiratory Medicine, Pudong New Area Peoples' Hospital Affiliated to Shanghai Health University, Shanghai, China.
Linxuan WangDepartment of Respiratory Medicine, Pudong New Area Peoples' Hospital Affiliated to Shanghai Health University, Shanghai, China.
Hua YangDepartment of Respiratory Medicine, Pudong New Area Peoples' Hospital Affiliated to Shanghai Health University, Shanghai, China.
Shanshan LiDepartment of Respiratory Medicine, Pudong New Area Peoples' Hospital Affiliated to Shanghai Health University, Shanghai, China.
Zhijun TangDepartment of Respiratory Medicine, Pudong New Area Peoples' Hospital Affiliated to Shanghai Health University, Shanghai, China.
Qiang LiDepartment of Respiratory Medicine, Changhai Hospital, Second Military Medical University, Shanghai, China.ORCID 0000-0002-8890-3786
Pudong New Area People's Hospital · CNSecond Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is a progressive lung disease that is primarily caused by cigarette smoke (CS)-induced chronic inflammation. In this study, we investigated the function and mechanism of action of the long non-coding RNA (lncRNA) taurine-up-regulated gene 1 (TUG1) in CS-induced COPD. We found that the expression of TUG1 was significantly higher in the sputum cells and lung tissues of patients with COPD as compared to that in non-smokers, and negatively correlated with the percentage of predicted forced expiratory volume in 1 second. In addition, up-regulation of TUG1 was observed in CS-exposed mice, and knockdown of TUG1 attenuated inflammation and airway remodelling in a mouse model. Moreover, TUG1 expression was higher in CS extract (CSE)-treated human bronchial epithelial cells and lung fibroblasts, whereas inhibition of TUG1 reversed CSE-induced inflammation and collagen deposition in vitro. Mechanistically, TUG1 promoted the expression of dual-specificity phosphatase 6 (DUSP6) by sponging miR-145-5p. DUSP6 overexpression reversed TUG1 knockdown-mediated inhibition of inflammation and airway remodelling. These findings suggested an important role of TUG1 in the pathological alterations associated with CS-mediated airway remodelling in COPD. Thus, TUG1 may be a promising therapeutic target in CS-induced airway inflammation and fibroblast activation.

Indexed as

Airway RemodelingAnimalsApoptosisCell ProliferationCells, CulturedCigarette SmokingDual Specificity Phosphatase 6FibroblastsHumansMiceMice, Inbred C57BLMicroRNAsPulmonary Disease, Chronic ObstructiveRNA, Long NoncodingDual Specificity Phosphatase 6DUSP6 protein, humanMicroRNAsMIRN145 microRNA, humanRNA, Long NoncodingTUG1 long noncoding RNA, humanairway inflammationairway remodellingCOPDDUSP6miR-145-5pTUG1

Identifiers

PMID31557398
PMCPMC6815828
OpenAlexW2976589164

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.