Evidence map›Paper›PMID 32519270›Full record

ArticleInflammation2020

KCNQ1OT1 Exacerbates Ischemia-Reperfusion Injury Through Targeted Inhibition of miR-140-3P.

Ming Yi, Yue Li, Dan Wang, Qiuxia Zhang, Li Yang, Chunsheng Yang

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.6field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 42 citations in OpenAlex.

  1. LncRNA KCNQ1OT1 aggravates myocardial ischemia/reperfusion injury by mediating the EZH2/TIMP-3 axis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
    Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. miR-140-5p and miR-140-3p: Key Actors in Aging-Related Diseases?International journal of molecular sciences · 2022
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Ming Yi *Department of Neurology, Tianjin Medical University General Hospital, 154 AnShan road, HePing District, Tianjin, 300052, China.
Yue Li *Department of Neurology, Tianjin Medical University General Hospital, 154 AnShan road, HePing District, Tianjin, 300052, China.
Dan WangDepartment of Clinical Laboratory, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, 300193, China.
Qiuxia ZhangDepartment of Neurology, Tianjin Medical University General Hospital, 154 AnShan road, HePing District, Tianjin, 300052, China.
Li YangDepartment of Neurology, Tianjin Medical University General Hospital, 154 AnShan road, HePing District, Tianjin, 300052, China.
Chunsheng YangDepartment of Neurology, Tianjin Medical University General Hospital, 154 AnShan road, HePing District, Tianjin, 300052, China. chunshengyang@163.com.ORCID http://orcid.org/0000-0002-3847-9526
Tianjin Medical University General Hospital · CNFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine · CN

Funding

National Natural Science Foundation of China 81571172
6 · The paper itself

Abstract

Potassium voltage-gated channel subfamily Q member 1 opposite strand 1 (KCNQ1OT1), a long non-coding RNA found in the KCNQ1 locus, has been evidenced to play important roles in the aggravation of inflammatory and oxidative stresses under hypoxia, but whether and how KCNQ1OT1 contributes to neuronal damages in the cerebral ischemic stroke remains unknown. In the present study, we found a dominant upregulation of KCNQ1OT1 both in the plasma of cerebral ischemia patients and in an oxygen-glucose deprivation and reperfusion (OGD/R) model in PC12 cells. KCNQ1OT1 knocking-down significantly ameliorated the inflammation, oxidative stress, and cell apoptosis induced by OGD/R. We further demonstrated that KCNQ1OT1 directly bound to and suppressed the expression of miR-140-3p. Overexpressing miR-140-3p significantly alleviated both the inflammation, oxidative stress, and cell apoptosis in OGD/R, while all those cytoprotective effects of miR-140-3p-overexpression were hindered by the co-overexpression of KCNQ1OT1. Furthermore, we found a direct interaction between miR-140-3p and the hypoxia-inducible factor-1α (HIF-1α), which was suppressed by the upregulation of KCNQ1OT1 in OGD/R. Our results indicate that KCNQ1OT1 exacerbates cerebral ischemia-reperfusion injury by targeted binding to miR-140-3p, thus interfering its direct interaction with HIF-1α. These data provide novel therapeutic targets in the cerebral ischemic stroke.

Indexed as

AnimalsBrain IschemiaGene Knockdown TechniquesHumansMicroRNAsPC12 CellsPotassium Channels, Voltage-GatedProtein BindingRatsReperfusion InjuryRNA, Small InterferingKCNQ1OT1 long non-coding RNA, humanMicroRNAsMirn140 microRNA, humanPotassium Channels, Voltage-GatedRNA, Small InterferingapoptosisHIF-1aischemia–reperfusion injuryKCNQ1OT1miR-140-3Poxidative stress

Identifiers

PMID32519270
OpenAlexW3033969962

What Socratic holds

Textmetadata
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 Socratic graph.