Evidence map›Paper›PMID 35291918›Full record

ArticleBioengineered2022

CDKN2B antisense RNA 1 expression alleviates idiopathic pulmonary fibrosis by functioning as a competing endogenouse RNA through the miR-199a-5p/Sestrin-2 axis.

Mei Yang, Egao Yin, Yiheng Xu, Yongjun Liu, Ting Li, Zhaoxing Dong, Wenlin Tai

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2022. 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
2.3field-weighted citation impact, top 11% 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, 15 citations in OpenAlex.

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  8. Crosstalk of ubiquitin system and non-coding RNA in fibrosis.International journal of biological sciences · 2024
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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 3 institutions in 1 country.

Mei YangDepartment of Respiration, The Sencond Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
Egao YinDepartment of Respiration, The Sencond Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
Yiheng XuDepartment of Clinical Laboratory, Yunnan Molecular Diagnostic Center, the Sencond Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
Yongjun LiuDepartment of Respiration, The Sencond Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
Ting LiDepartment of Respiration, Hwa Mei Hospital, University of Chinese Academy of Sciences, Ningbo, Zhejiang, China.
Zhaoxing DongDepartment of Respiration, Hwa Mei Hospital, University of Chinese Academy of Sciences, Ningbo, Zhejiang, China.
Wenlin TaiDepartment of Clinical Laboratory, Yunnan Molecular Diagnostic Center, the Sencond Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
Kunming Medical University · CNUniversity of Chinese Academy of Sciences · CNYunnan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is an idiopathic interstitial lung disease. At present, the pathogenesis of IPF has not been fully elucidated, which has affected the development of effective treatment methods. Here, we explored the function and potential mechanism of long noncoding RNA (lncRNA) CDKN2B antisense RNA 1 (CDKN2B-AS1) in IPF.Transforming growth factor-β (TGF-β) and bleomycin (BLM) were used to induce IPF in cells and animal models. Real Time quantitative Polymerase Chain Reaction (RT-qPCR) showed the expression of CDKN2B-AS1, miR-199a-5p and Sestrin-2 (SESN2) in cells and tissues. The double luciferase reporter gene assay confirmed the targeting relationship among CDKN2B-AS1, miR-199a-5p, and SESN2. Related protein levels were detected by Western blot combined with Cell Counting Kit-8 (CCK-8), wound healing, and flow cytometry to analyze cell proliferation, migration, and apoptosis. The pathological characteristics of mouse lung tissue were determined by Hematoxylin-eosin (HE) and Masson staining. We found that the expression of CDKN2B-AS1 was decreased in TGF-β-treated cells and BLM-treated mice. Overexpression of CDKN2B-AS1 inhibited cell proliferation and migration, promoted apoptosis, decreased the expression of fibrosis-related proteins and promoted autophagy. In addition, overexpression of CDKN2B-AS1 alleviated pulmonary fibrosis in BLM-treated mice. Mechanistically, CDKN2B-AS1 acts as a miR-199a-5p sponge to regulate SESN2 expression. Our results indicate the importance of the CDKN2B-AS1/miR-199a-5p/SESN2 axis.

Indexed as

Idiopathic Pulmonary FibrosisMicroRNAsRNA, Long NoncodingAnimalsCell Line, TumorCell ProliferationMiceRNA, AntisenseTransforming Growth Factor betaMicroRNAsRNA, AntisenseRNA, Long NoncodingTransforming Growth Factor betaautophagyCDKN2B-AS1IPFmiR-199a-5pSESN2

Identifiers

PMID35291918
PMCPMC9208479
OpenAlexW4220902941

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.