Evidence map›Paper›PMID 31734557›Full record

ArticleMolecular therapy. Nucleic acids2019

Inhibition of lncRNA XIST Improves Myocardial I/R Injury by Targeting miR-133a through Inhibition of Autophagy and Regulation of SOCS2.

Zhiqiang Li, Yaping Zhang, Nan Ding, Yudong Zhao, Zankai Ye, Lei Shen, Hanlu Yi, Yaobin Zhu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular therapy. Nucleic acids, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

47 citing papers in PubMed, 70 citations in OpenAlex.

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  13. The Role of Long Non-Coding RNAs in Cardiovascular Diseases.International journal of molecular sciences · 2023
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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

8 authors at 3 institutions in 1 country.

Zhiqiang LiDepartment of Cardiovascular Surgery, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing 100045, China.
Yaping ZhangDepartment of Heart Center, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China.
Nan DingDepartment of Cardiovascular Surgery, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing 100045, China.
Yudong ZhaoDepartment of Cardiovascular Surgery, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing 100045, China.
Zankai YeDepartment of Cardiovascular Surgery, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing 100045, China.
Lei ShenDepartment of Cardiovascular Surgery, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing 100045, China.
Hanlu YiDepartment of Cardiovascular Surgery, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing 100045, China.
Yaobin ZhuDepartment of Cardiovascular Surgery, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing 100045, China. Electronic address: chongdejia8865na@126.com.
Beijing Children’s Hospital · CNCapital Medical University · CNBeijing Friendship Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The objective of this study was to investigate the role of lncRNA XIST and its relationship with miR-133a in myocardial I/R injury. H9C2 cells treated by hypoxia/reoxygenation (H/R) were used to establish an in vitro I/R model. The small interfering RNA (siRNA) for XIST and miR-133 mimics, inhibitor, and suppressor of cytokine signaling (SOCS2) recombinant plasmids were used to transfect the cells. Cell apoptosis was determined by flow cytometry analysis, and cell viability was used for 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide, Thiazolyl Blue Tetrazolium Bromide (MTT) assay. The dual-luciferase reporter assay was performed to confirm binding between XIST and miR-133a, as well as miR-133a and SOCS2. To inhibit or overexpress XIST, miR-133a, or SOCS2 in I/R mice, we used recombinant lentivirus vectors and adenovirus vectors for tail vein injection. The expression of XIST, miR-133a, and SOCS2 was determined by quantitative real-time PCR, and LC3 I/II and Beclin1 was determined by western blotting. The expression of XIST and SOCS2 was significantly upregulated, whereas the miR-133a level was remarkably downregulated in both H/R H9C2 cells and I/R mice myocardial tissues. In both H/R H9C2 cells and I/R mice, the inhibition of XIST led to decreased apoptosis and autophagy, and inhibition of miR-133a reversed these effects. Similarly, overexpression of miR-133a resulted in reduced apoptosis and autophagy, which were reversed by overexpression of SOCS2. The inhibition of XIST and overexpression of miR-133a also promote cell viability of H/R cells. The dual-luciferase reporter assay significantly showed that XIST directly targeted on miR-133a, and miR-133a directly targeted on SOCS2. The inhibition of XIST could improve myocardial I/R injury by regulation of the miR-133a/SOCS2 axis and inhibition of autophagy.

Indexed as

autophagylncRNA XISTmiR-133amyocardial ischemic-reperfusion injurySOCS2

Identifiers

PMID31734557
PMCPMC6861669
OpenAlexW2980004317

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.