Evidence map›Paper›PMID 30684280›Full record

ArticleJournal of cellular physiology2019

LINC00520 targeting miR-27b-3p regulates OSMR expression level to promote acute kidney injury development through the PI3K/AKT signaling pathway.

Xinghan Tian, Yongqiang Ji, Yafeng Liang, Jing Zhang, Lina Guan, Chunting Wang

Abstract read
In one paragraph

Article in Journal of cellular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

42 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
  2. Article
  3. The role of PI3K/Akt signaling pathway in chronic kidney disease.International urology and nephrology · 2024
    Review
  4. Article
  5. Article
  6. Review
  7. Exosomes promote hFOB1.19 proliferation and differentiation via LINC00520.Journal of orthopaedic surgery and research · 2023
    Article
  8. Review
  9. Article
  10. Article
  11. MicroRNAs in kidney injury and disease.Nature reviews. Nephrology · 2022
    Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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

6 authors at 2 institutions in 1 country.

Xinghan TianDepartment of Critical Care Medicine, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, China.
Yongqiang JiDepartment of Nephrology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong, China.
Yafeng LiangDepartment of Critical Care Medicine, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong, China.
Jing ZhangDepartment of Critical Care Medicine, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, China.
Lina GuanDepartment of Neurology Intensive Care Unit, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong, China.ORCID http://orcid.org/0000-0003-1123-6695
Chunting WangDepartment of Critical Care Medicine, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, China.
Qingdao University · CNShandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute kidney injury (AKI) shows several kinds of disorders, which acutely harm the kidney. However, the current medical methods have limited therapeutic effects. The present study aimed to find out the molecular mechanism of AKI pathogenesis, which may provide new insights for future therapy.

methodsBioinformatic analysis was conducted using the R language (AT&T BellLaboratories, University of Auckland, New Zealand) to acquire the differentially expressed long noncoding RNAs (lncRNAs) and messenger RNAs (mRNAs) in AKI. The expression levels of RNAs and related proteins in tissues and cells were detected by quantitative real-time PCR (qRT-PCR) and western blot. Dual-luciferase reporter gene assays were performed to verify the target relationship between microRNA (miRNA) and lncRNA as well as miRNA and mRNA. Flow cytometry and tunnel assay were used to detect the cell apoptotic rate in AKI.

resultsLINC00520, miR-27b-3p, and OSMR form an axis to regulate AKI. Knockdown of LINC00520 reduced acute renal injury both in vitro and in vivo. LINC00520 activated the PI3K/AKT pathway to aggravate renal ischemia/reperfusion injury, while upregulation of miR-27b-3p or downregulation of OSMR could accelerate the recovery of AKI.

conclusionOverexpression of LINC00520 contributes to the aggravation of AKI by targeting miR-27b-3p/ OSMR.

Indexed as

Acute Kidney InjuryAnimalsCell LineCell ProliferationGene Expression RegulationGene Knockdown TechniquesHumansMicroRNAsOncogene Protein v-aktOncostatin M Receptor beta SubunitPhosphatidylinositol 3-KinasesRatsRNA, Long NoncodingSignal TransductionMicroRNAsMIRN27 microRNA, humanOncogene Protein v-aktOncostatin M Receptor beta SubunitOSMR protein, humanPhosphatidylinositol 3-KinasesRNA, Long Noncodingacute kidney injuryLINC00520miR-27b-3pOSMRPI3K-AKT

Identifiers

PMID30684280
PMCPMC13483068
OpenAlexW2914342447

What OpenQuestion holds

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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.