Evidence map›Paper›PMID 29411215›Full record

ArticleInflammation2018

The lncRNA H19 Mediates Pulmonary Fibrosis by Regulating the miR-196a/COL1A1 Axis.

Qingchun Lu, Zhongliang Guo, Wang Xie, Wenjing Jin, Dongyi Zhu, Song Chen, Tao Ren

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

54 citing papers in PubMed, 99 citations in OpenAlex.

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  13. Serum non-coding RNAs for diagnosis and stage of liver fibrosis.Journal of clinical laboratory analysis · 2022
    Review
  14. Article
  15. Article
  16. The Long Noncoding RNADNA and cell biology · 2022
    Article
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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 4 institutions in 1 country.

Qingchun LuDepartment of Respiratory Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 200120, China.
Zhongliang GuoDepartment of Respiratory Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 200120, China.
Wang XieDepartment of Respiratory Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 200120, China.
Wenjing JinDepartment of Intensive Care Unit, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, 201399, China.
Dongyi ZhuDepartment of Respiratory Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 200120, China.
Song ChenDepartment of Emergency and Critical Care Medicine, Shanghai Pudong New Area People's Hospital, Shanghai, 201299, China.
Tao RenDepartment of Respiratory Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, 200233, China. rentaosh@126.com.ORCID http://orcid.org/0000-0003-0845-3058
Shanghai East Hospital · CNFudan University · CNPudong New Area People's Hospital · CNShanghai Jiao Tong University · CN

Funding

National Key R&D Plan 2017YFA0104600National Natural Science Foundation of China 81370174National Natural Science Foundation of China 81372347National Natural Science Foundation of China 81673014Outstanding Academic Leaders Plan of Shanghai Municipal Science and Technology Committee 16XD1403100
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is characterized by lung fibroblasts accumulation and extracellular matrix (ECM) deposition. Recently, long-noncoding RNAs (lncRNAs) have emerged as critical regulators and prognostic markers in several diseases including IPF. In the present study, we found that the expression of H19 was significantly increased in transforming growth factor-β (TGF-β)-induced fibroblast proliferation and bleomycin-(BLM) induced lung fibrosis (p < 0.05). We further demonstrated that H19 was a direct target of miR-196a and was associated with COL1A1 expression by sponging miR-196a. Moreover, downregulation of H19 alleviated fibroblast activation and lung fibrosis, and this effect was blocked by a miR-196a inhibitor. In conclusion, our results suggest that lncRNA H19 has a promotive effect on BLM-induced IPF, and it functions as a molecular sponge of miR-196a, which provides a novel therapeutic target for IPF.

Indexed as

AnimalsBleomycinCell ProliferationCollagen Type ICollagen Type I, alpha 1 ChainExtracellular MatrixFibroblastsHumansIdiopathic Pulmonary FibrosisMiceMicroRNAsRNA, Long NoncodingBleomycinCollagen Type ICollagen Type I, alpha 1 ChainH19 long non-coding RNAMicroRNAsMIRN196 microRNA, mouseRNA, Long NoncodingCOL1A1competing endogenous RNAH19long noncoding RNAlung fibrosismiR-196a

Identifiers

PMID29411215
OpenAlexW2786224552

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.