Evidence map›Paper›PMID 28316060›Full record

ArticleMolecular and cellular biochemistry2017

HOTAIR functions as a competing endogenous RNA to regulate PTEN expression by inhibiting miR-19 in cardiac hypertrophy.

Yanjun Lai, Shuai He, Liming Ma, Hong Lin, Biyun Ren, Jing Ma, Xinyu Zhu, Shifang Zhuang

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
–field-weighted citation impact
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

55 citing papers in PubMed.

  1. Trial
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  7. Article
  8. lncRNA HOTAIR and Cardiovascular diseases.Functional & integrative genomics · 2024
    Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Long Non-Coding RNAs in Cardiac Hypertrophy.Frontiers in molecular medicine · 2022
    Review
  18. Article
  19. Review
  20. Review
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.

Yanjun LaiDepartment of Clinical Laboratory, Ninth Hospital of Xi'an, 151 East of South Second Ring Road, Xi'an, 710003, Shaanxi, China.
Shuai HeDepartment of Clinical Laboratory, Ninth Hospital of Xi'an, 151 East of South Second Ring Road, Xi'an, 710003, Shaanxi, China.
Liming MaDepartment of Clinical Laboratory, Ninth Hospital of Xi'an, 151 East of South Second Ring Road, Xi'an, 710003, Shaanxi, China. lmma_xa@21cn.com.
Hong LinDepartment of Clinical Laboratory, Ninth Hospital of Xi'an, 151 East of South Second Ring Road, Xi'an, 710003, Shaanxi, China.
Biyun RenDepartment of Clinical Laboratory, Ninth Hospital of Xi'an, 151 East of South Second Ring Road, Xi'an, 710003, Shaanxi, China.
Jing MaDepartment of Clinical Laboratory, Ninth Hospital of Xi'an, 151 East of South Second Ring Road, Xi'an, 710003, Shaanxi, China.
Xinyu ZhuDepartment of Clinical Laboratory, Ninth Hospital of Xi'an, 151 East of South Second Ring Road, Xi'an, 710003, Shaanxi, China.
Shifang ZhuangDepartment of Clinical Laboratory, Ninth Hospital of Xi'an, 151 East of South Second Ring Road, Xi'an, 710003, Shaanxi, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sustained cardiac hypertrophy (CH) is related to a variety of physiological as well as pathological stimuli and eventually increases the risk of heart failure. HOTAIR has been identified as a competing endogenous RNA in multiple human biological processes. Whether lncRNA-HOTAIR is involved in the progress of CH and how it works still remain unknown. Herein, we found that HOTAIR was down-regulated, while miR-19 was up-regulated in both heart tissues from TAC-operated mice in vivo and cultural cardiomyocytes treated with Ang-II in vitro by real-time PCR. Meanwhile, HOTAIR expression was negatively correlated with miR-19 in TAC-operated mice. HOTAIR overexpression reduced cell surface area and the expression of hypertrophic markers ANP, BNP, and β-MHC in response to Ang-II stimulation as well as knockdown of miR-19. The further molecular mechanisms of HOTAIR action in CH demonstrated that HOTAIR may act as a competing endogenous RNA (ceRNA) for miR-19, thereby modulating the dis-inhibition of its endogenous target PTEN and playing an important role in inhibiting CH progress. These findings reveal a novel function of LncRNAs, which conduce to an extensive understanding of CH and provide novel research directions and therapeutic options for treating this disease.

Indexed as

Gene Expression Regulation, EnzymologicAnimalsCardiomegalyMaleMiceMicroRNAsPTEN PhosphohydrolaseRNA, Long NoncodingHOTAIR long non-coding RNA, mouseMicroRNAsMIRN19 microRNA, mousePTEN PhosphohydrolasePten protein, mouseRNA, Long NoncodingCardiac hypertrophyCompeting endogenous RNAHOTAIRMiR-19PTEN

Identifiers

PMID28316060

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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.