Evidence map›Paper›PMID 34517790›Full record

ArticleBioengineered2021

Circular RNA SMEK1 promotes neuropathic pain in rats through targeting microRNA-216a-5p to mediate Thioredoxin Interacting Protein (TXNIP) expression.

Yufu Xin, Xinrong Song, Qingye Ge

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

15 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. The role of non-coding RNAs in neuropathic pain.Pflugers Archiv : European journal of physiology · 2024
    Review
  7. Review
  8. The roles of circular RNAs in nerve injury and repair.Frontiers in molecular neuroscience · 2024
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. DNA Methylation and Non-Coding RNAs during Tissue-Injury Associated Pain.International journal of molecular sciences · 2022
    Review
  14. Article
  15. 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

3 authors at 2 institutions in 1 country.

Yufu XinDepartment of Rehabilitation Medicine, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang City, Henan Province, 471000, China.
Xinrong SongDepartment of Rehabilitation Medicine, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang City, Henan Province, 471000, China.
Qingye GeDepartment of Rehabilitation Medicine of Chinese Medicine Hospital of PuYang Henan, Puyang City, Henan Province, 457000, China.
First Affiliated Hospital of Henan University of Science and Technology · CNAnyang Hospital of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuropathic pain (NP) is a disease induced by damage to the nervous system. A large number of studies have manifested that circular RNAs (circRNAs) are key in the development of neurological diseases. However, the role of circRNA in NP remains ambiguous. In this study, the biological function and molecular mechanism of circSMEK1 were investigated in NP. NP rat and cell models were established by chronic contractile injury (CCI) surgery and lipopolysaccharide (LPS) treatment, separately. The results exposed that circSMEK1 and TXNIP were up-regulated in NP, while miR-216a-5p was down-regulated. The claw retraction threshold and claw retraction latency in rats were elevated and reduced separately via knockdown circSMEK1 and miR-216a-5p. Meanwhile, knockout circSMEK1 or elevated miR-216a-5p declined inflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL6 in spinal cord, and the activation of microglia, but promoted the polarization of microglia into anti-inflammatory type, while up-regulation of circSMEK1 or knockdown of miR-216a-5p was opposite. Mechanism studies demonstrated that circSMEK1 mediated TXNIP expression through competitive adsorption of miR-216a-5p. Functional rescue experiments manifested that the suppressive effect of circSMEK1 knockdown on NP was reversed by declined miR-216a-5p simultaneously. In conclusion, the results of this study affirmed that circSMEK1 facilitates NP inflammation and microglia M1 polarization by modulating miR-216a-5p/TXNIP axis, providing a new molecular target for the future treatment of NP.

Indexed as

NeuralgiaAnimalsBehavior, AnimalCell Cycle ProteinsCell LineMaleMicrogliaMicroRNAsRatsRats, Sprague-DawleyRNA, CircularCell Cycle ProteinsMicroRNAsMIRN216 microRNA, ratRNA, CircularTXNIP protein, ratCircSMEK1inflammationmicrogliaMicroRNA-216a-5pneuropathic pain

Identifiers

PMID34517790
PMCPMC8806878
OpenAlexW3200520830

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Registered trials

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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.