Evidence map›Paper›PMID 31868202›Full record

ArticleBioscience reports2020

STAT3-induced up-regulation of lncRNA NEAT1 as a ceRNA facilitates abdominal aortic aneurysm formation by elevating TULP3.

Bing Cai, Baihui Yang, Dong Huang, Di Wang, Jun Tian, Feiyun Chen, Xi Wang

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Biology · 2025
    Article
  3. Emerging Roles of Long Non-Coding RNAs in Cardiovascular Diseases.Journal of cellular and molecular medicine · 2025
    Review
  4. Article
  5. The roles of long noncoding RNA NEAT1 in cardiovascular diseases.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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 1 institution in 1 country.

Bing CaiCardiovascular Surgery, Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, 650101, China.
Baihui YangCardiovascular Surgery, Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, 650101, China.
Dong HuangCardiovascular Surgery, Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, 650101, China.
Di WangCardiovascular Surgery, Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, 650101, China.
Jun TianCardiovascular Surgery, Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, 650101, China.
Feiyun ChenCardiovascular Surgery, Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, 650101, China.
Xi WangCardiovascular Surgery, Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, 650101, China.
Kunming Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long noncoding RNAs (lncRNAs) were viewed as crucial participants in the pathogenesis of abdominal aortic aneurysm (AAA). LncRNA NEAT1 was recognized as an oncogenic gene in various diseases. However, its function and mechanism in AAA were not precisely documented. Here, we explored the functional role and molecular mechanism of NEAT1 in AAA. Functionally, the effect of NEAT1 on the proliferation was assessed by CCK-8 and EdU assay, while its impact on the apoptosis was evaluated through caspase-3/9 activity and TUNEL assays. As a result, we found that NEAT1 knockdown enhanced the proliferation and impaired the apoptosis of vascular smooth muscle cells (VSMCs). Reversely, overexpressed NEAT1 exerted anti-proliferation and pro-apoptosis effects in VSMCs. Mechanically, we found that STAT3 acted as a transcription factor and contributed to NEAT1 transcription by ChIP and luciferase reporter assays. In addition, NEAT1 was confirmed as a sponge of miR-4688 and thereby increase the expression of TULP3 in VSMCs via RIP assay and RNA pull-down assay. Rescue experiments indicted that TULP3 overexpressing countervailed the impact of NEAT1 depletion on AAA biological processes. Conclusively, lncRNA NEAT1 induced by STAT3 was identified as a ceRNA and facilitated AAA formation by targeting miR-4688/TULP3 axis.

Indexed as

Vascular RemodelingAortic Aneurysm, AbdominalApoptosisCell ProliferationCells, CulturedHumansIntracellular Signaling Peptides and ProteinsMicroRNAsMuscle, Smooth, VascularMyocytes, Smooth MuscleRNA, Long NoncodingSignal TransductionSTAT3 Transcription FactorUp-RegulationIntracellular Signaling Peptides and ProteinsMicroRNAsNEAT1 long non-coding RNA, humanRNA, Long NoncodingSTAT3 protein, humanSTAT3 Transcription FactorTULP3 protein, humanAAAmiR-4688NEAT1STAT3TULP3

Identifiers

PMID31868202
PMCPMC6960067
OpenAlexW2996980852

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.