Evidence map›Paper›PMID 29248830›Full record

ArticleRedox biology2018

miR-200a-5p regulates myocardial necroptosis induced by Se deficiency via targeting RNF11.

Tianshu Yang, Changyu Cao, Jie Yang, Tianqi Liu, Xin Gen Lei, Ziwei Zhang, Shiwen Xu

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
7.5field-weighted citation impact, top 1% 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

51 citing papers in PubMed, 143 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Observational
  16. Article
  17. Article
  18. Article
  19. Article
  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

7 authors at 2 institutions in 2 countries.

Tianshu YangNortheast Agricultural University, Harbin 150030, PR China.
Changyu CaoNortheast Agricultural University, Harbin 150030, PR China.
Jie YangNortheast Agricultural University, Harbin 150030, PR China.
Tianqi LiuNortheast Agricultural University, Harbin 150030, PR China.
Xin Gen LeiDepartment of Animal Science, Cornell University, Ithaca, NY, United States. Electronic address: xl20@cornell.edu.
Ziwei ZhangNortheast Agricultural University, Harbin 150030, PR China; Key Laboratory of Animal Cellular and Genetic Engineering of Heilongjiang Province, Northeast Agricultural University, Harbin 150030, PR China. Electronic address: zhangziwei@neau.edu.cn.
Shiwen XuNortheast Agricultural University, Harbin 150030, PR China; Key Laboratory of Animal Cellular and Genetic Engineering of Heilongjiang Province, Northeast Agricultural University, Harbin 150030, PR China. Electronic address: shiwenxu@neau.edu.cn.
Northeast Agricultural University · CNCornell University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Necroptosis has been discovered as a new paradigm of cell death and may play a key role in heart disease and selenium (Se) deficiency. Hence, we detected the specific microRNA (miRNA) in response to Se-deficient heart using microRNAome analysis. For high-throughput sequencing using Se-deficient chicken cardiac tissue, we selected miR-200a-5p and its target gene ring finger protein 11 (RNF11) based on differential expression in cardiac tissue and confirmed the relationship between miR-200a-5p and RNF11 by dual luciferase reporter assay and real-time quantitative PCR (qRT-PCR) in cardiomyocytes. We further explored the function of miR-200a-5p and observed that overexpression of miR-200a-5p spark the receptor interacting serine/threonine kinase 3 (RIP3)-dependent necroptosis in vivo and in vitro. To understand whether miR-200a-5p and RNF11 are involved in the RIP3-dependent necroptosis pathway, we presumed that oxidative stress, inflammation response and the mitogen-activated protein kinase (MAPK) pathway might trigger necroptosis. Interestingly, necroptosis trigger, z-VAD-fmk, failed to induce necroptosis but enhanced cell survival against necrosis in cardiomyocytes with knockdown of miR-200a-5p. Our present study provides a new insight that the modulation of miR-200a-5p and its target gene might block necroptosis in the heart, revealing a novel myocardial necrosis regulation model in heart disease.

Indexed as

AnimalsApoptosisCarrier ProteinsChickensDNA-Binding ProteinsHumansMicroRNAsMyocardial Reperfusion InjuryMyocardiumMyocytes, CardiacNecrosisOxidative StressReactive Oxygen SpeciesSeleniumCarrier ProteinsDNA-Binding ProteinsMicroRNAsReactive Oxygen SpeciesRNF11 protein, humanSeleniumCardiomyocytesmiR-200a-5pNecroptosisRNF11Selenium

Identifiers

PMID29248830
PMCPMC5975215
OpenAlexW2772227821

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.