Evidence map›Paper›PMID 34547172›Full record

ArticleJournal of cellular and molecular medicine2021

LncRNA TUG1 attenuates ischaemia-reperfusion-induced apoptosis of renal tubular epithelial cells by sponging miR-144-3p via targeting Nrf2.

Sheng Zhao, Wu Chen, Wei Li, Weimin Yu, Siqi Li, Ting Rao, Yuan Ruan, Xiangjun Zhou, Cong Liu, Yucheng Qi and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 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
1.0field-weighted citation impact, top 29% 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. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. NRF2 Dysregulation and Therapeutic Insights Across Chronic Kidney Diseases.International journal of molecular sciences · 2025
    Review
  7. lncRNA TUG1 and kidney diseases.BMC nephrology · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  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

11 authors at 1 institution in 1 country.

Sheng ZhaoDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, China.
Wu ChenDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, China.ORCID 0000-0002-0672-2122
Wei LiDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, China.
Weimin YuDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, China.
Siqi LiDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, China.
Ting RaoDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, China.
Yuan RuanDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, China.
Xiangjun ZhouDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, China.
Cong LiuDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, China.
Yucheng QiDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, China.
Fan ChengDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, China.ORCID 0000-0002-3471-6221
Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal ischaemia/reperfusion (I/R) injury may induce kidney damage and dysfunction, in which oxidative stress and apoptosis play important roles. Long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) are reported to be closely related to renal I/R, but the specific molecular mechanism is still unclear. The purpose of this research was to explore the regulatory effect of lncRNA TUG1 on oxidative stress and apoptosis in renal I/R injury. This research revealed that in renal I/R injury and hypoxia/reperfusion (H/R) injury in vitro, the expression level of lncRNA TUG1 was upregulated, and oxidative stress levels and apoptosis levels were negatively correlated with the expression level of lncRNA TUG1. Using bioinformatics databases such as TargetScan and microRNA.org, microRNA-144-3p (miR-144-3p) was predicted to be involved in the association between lncRNA TUG1 and Nrf2. This study confirmed that the level of miR-144-3p was significantly reduced following renal I/R injury and H/R injury in vitro, and miR-144-3p was determined to target Nrf2 and inhibit its expression. In addition, lncRNA TUG1 can reduce the inhibitory effect of miR-144-3p on Nrf2 by sponging miR-144-3p. In summary, our research shows that lncRNA TUG1 regulates oxidative stress and apoptosis during renal I/R injury through the miR-144-3p/Nrf2 axis, which may be a new treatment target for renal I/R injury.

Indexed as

AnimalsApoptosisBiomarkersCell LineDisease Models, AnimalDisease SusceptibilityEndoplasmic Reticulum StressEpithelial CellsGene Expression ProfilingGene Expression RegulationGene Knockout TechniquesKidney DiseasesKidney TubulesMaleMiceMicroRNAsBiomarkerslong non-coding RNA TUG1, mouseMicroRNAsMIRN144 microRNA, mouseNF-E2-Related Factor 2Reactive Oxygen SpeciesRNA, Long NoncodingapoptosisLncRNA TUG1miR-144-3pNrf2renal ischaemia/reperfusion injury

Identifiers

PMID34547172
PMCPMC8505827
OpenAlexW3199150407

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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.