Evidence map›Paper›PMID 23226300›Full record

ArticlePloS one2012

miR-1 exacerbates cardiac ischemia-reperfusion injury in mouse models.

Zhenwei Pan, Xuelin Sun, Jinshuai Ren, Xin Li, Xu Gao, Chunying Lu, Yang Zhang, Hui Sun, Ying Wang, Huimin Wang and 4 more

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

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

81 citing papers in PubMed, 122 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. The interplay of hydrogen sulfide and microRNAs in cardiovascular diseases: insights and future perspectives.Mammalian genome : official journal of the International Mammalian Genome Society · 2024
    Review
  10. Review
  11. Article
  12. The important role of miR-1-3p in cancers.Journal of translational medicine · 2023
    Review
  13. Article
  14. Cripto Is Targeted by miR-1a-3p in a Mouse Model of Heart Development.International journal of molecular sciences · 2023
    Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Review

21 more citing papers are in PubMed but not listed here.

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

14 authors at 1 institution in 1 country.

Zhenwei PanDepartment of Pharmacology-Key Laboratory of Cardiovascular Medicine Research, Ministry of Education, State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Harbin Medical University, Harbin, Heilongjiang, People's Republic of China. panzw@ems.hrbmu.edu.cn
Xuelin Sun
Jinshuai Ren
Xin Li
Xu Gao
Chunying Lu
Yang Zhang
Hui Sun
Ying Wang
Huimin Wang
Jinghao Wang
Liangjun Xie
Yanjie Lu
Baofeng Yang
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have revealed the critical role of microRNAs (miRNAs) in regulating cardiac injury. Among them, the cardiac enriched microRNA-1(miR-1) has been extensively investigated and proven to be detrimental to cardiac myocytes. However, solid in vivo evidence for the role of miR-1 in cardiac injury is still missing and the potential therapeutic advantages of systemic knockdown of miR-1 expression remained unexplored. In this study, miR-1 transgenic (miR-1 Tg) mice and locked nucleic acid modified oligonucleotide against miR-1 (LNA-antimiR-1) were used to explore the effects of miR-1 on cardiac ischemia/reperfusion injury (30 min ischemia followed by 24 h reperfusion). The cardiac miR-1 level was significantly increased in miR-1 Tg mice, and suppressed in LNA-antimiR-1 treated mice. When subjected to ischemia/reperfusion injury, miR-1 overexpression exacerbated cardiac injury, manifested by increased LDH, CK levels, caspase-3 expression, apoptosis and cardiac infarct area. On the contrary, LNA-antimiR-1 treatment significantly attenuated cardiac ischemia/reperfusion injury. The expression of PKCε and HSP60 was significantly repressed by miR-1 and enhanced by miR-1 knockdown, which may be a molecular mechanism for the role miR-1 in cardiac injury. Moreover, luciferase assay confirmed the direct regulation of miR-1 on protein kinase C epsilon (PKCε) and heat shock protein 60 (HSP60). In summary, this study demonstrated that miR-1 is a causal factor for cardiac injury and systemic LNA-antimiR-1 therapy is effective in ameliorating the problem.

Indexed as

AnimalsApoptosisBase SequenceCaspase 3Chaperonin 60Creatine KinaseDisease Models, AnimalGene Expression RegulationGene Knockdown TechniquesHumansL-Lactate DehydrogenaseMaleMiceMice, Inbred C57BLMice, TransgenicMicroRNAsCaspase 3Chaperonin 60Creatine KinaseL-Lactate Dehydrogenaselocked nucleic acidMicroRNAsMirn1 microRNA, mouseOligonucleotidesProtein Kinase C-epsilon

Identifiers

PMID23226300
PMCPMC3511560
OpenAlexW2038618647

What OpenQuestion holds

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LicenceCC BY
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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.