Evidence map›Paper›PMID 23543060›Full record

ArticleThe Journal of clinical investigation2013

MicroRNA-26 governs profibrillatory inward-rectifier potassium current changes in atrial fibrillation.

Xiaobin Luo, Zhenwei Pan, Hongli Shan, Jiening Xiao, Xuelin Sun, Ning Wang, Huixian Lin, Ling Xiao, Ange Maguy, Xiao-Yan Qi and 13 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 152 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
152citing papers in PubMed, 2 pooled it
15.5field-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

152 citing papers in PubMed, 2 syntheses or guidelines pooled it, 264 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Time's imprint on the left atrium: aging and atrial myopathy.The journal of cardiovascular aging · 2025
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Animal and cellular models of atrial fibrillation: a review.Frontiers in cardiovascular medicine · 2025
    Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. The network of cardiac KNaunyn-Schmiedeberg's archives of pharmacology · 2024
    Review

92 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

23 authors at 2 institutions in 2 countries.

Xiaobin LuoResearch Center, Montreal Heart Institute, Montreal, Quebec, Canada.
Zhenwei Pan
Hongli Shan
Jiening Xiao
Xuelin Sun
Ning Wang
Huixian Lin
Ling Xiao
Ange Maguy
Xiao-Yan Qi
Yue Li
Xu Gao
Deli Dong
Yong Zhang
Yunlong Bai
Jing Ai
Lihua Sun
Hang Lu
Xiao-Yan Luo
Zhiguo Wang
Yanjie Lu
Baofeng Yang
Stanley Nattel
Harbin Medical University · CNMontreal Heart Institute · CA

Funding

Canadian Institutes of Health Research MOP 44365
6 · The paper itself

Abstract

Atrial fibrillation (AF) is a highly prevalent arrhythmia with pronounced morbidity and mortality. Inward-rectifier K+ current (IK1) is believed to be an important regulator of reentrant-spiral dynamics and a major component of AF-related electrical remodeling. MicroRNA-26 (miR-26) is predicted to target the gene encoding KIR2.1, KCNJ2. We found that miR-26 was downregulated in atrial samples from AF animals and patients and this downregulation was accompanied by upregulation of IK1/KIR2.1 protein. miR-26 overexpression suppressed expression of KCNJ2/KIR2.1. In contrast, miR-26 knockdown, inhibition, or binding-site mutation enhanced KCNJ2/KIR2.1 expression, establishing KCNJ2 as a miR-26 target. Knockdown of endogenous miR-26 promoted AF in mice, whereas adenovirus-mediated expression of miR-26 reduced AF vulnerability. Kcnj2-specific miR-masks eliminated miR-26-mediated reductions in Kcnj2, abolishing miR-26's protective effects, while coinjection of a Kcnj2-specific miR-mimic prevented miR-26 knockdown-associated AF in mice. Nuclear factor of activated T cells (NFAT), a known actor in AF-associated remodeling, was found to negatively regulate miR-26 transcription. Our results demonstrate that miR-26 controls the expression of KCNJ2 and suggest that this downregulation may promote AF.

Indexed as

Gene Expression RegulationAnimalsAtrial FibrillationBinding SitesCells, CulturedDogsDown-RegulationFemaleHumansMaleMiceMice, Inbred C57BLMicroRNAsMutationMyocytes, CardiacNFATC Transcription FactorsKCNJ2 protein, humanKCNJ2 protein, ratKir2.1 channelMicroRNAsMIRN26 microRNA, humanMirn26 microRNA, mouseMIRN26 microRNA, ratNFATC Transcription FactorsPotassiumPotassium Channels, Inwardly Rectifying

Identifiers

PMID23543060
PMCPMC3635715
OpenAlexW2032138405

What OpenQuestion 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 OpenQuestion graph.