Evidence map›Paper›PMID 29700282›Full record

ArticleCell death & disease2018

LincRNA 1700020I14Rik alleviates cell proliferation and fibrosis in diabetic nephropathy via miR-34a-5p/Sirt1/HIF-1α signaling.

Ailing Li, Rui Peng, Yan Sun, Handeng Liu, Huimin Peng, Zheng Zhang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
5.7field-weighted citation impact, top 2% 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

104 citing papers in PubMed, 158 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. WTAP-induced mCell biochemistry and biophysics · 2025
    Article
  6. Long non-coding RNAMolecular therapy. Nucleic acids · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

44 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

6 authors at 2 institutions in 1 country.

Ailing LiMolecular Medicine and Cancer Research Center, Chongqing Medical University, 400016, Chongqing, China.
Rui PengDepartment of Bioinformatics, Chongqing Medical University, 400016, Chongqing, China.
Yan SunMolecular Medicine and Cancer Research Center, Chongqing Medical University, 400016, Chongqing, China.
Handeng LiuMolecular Medicine and Cancer Research Center, Chongqing Medical University, 400016, Chongqing, China.
Huimin PengMolecular Medicine and Cancer Research Center, Chongqing Medical University, 400016, Chongqing, China.
Zheng ZhangMolecular Medicine and Cancer Research Center, Chongqing Medical University, 400016, Chongqing, China. zhangzheng92@163.com.ORCID 0000-0002-0062-517X
Chongqing Medical University · CNRongcheng City People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long intergenic noncoding RNAs (lincRNAs) have been gradually identified to be functional in a variety of different mechanisms associating with development and epigenetic regulation of cellular homeostasis. However, the study of lincRNAs in diabetic nephropathy (DN) is still in its infancy. Here, we have found dysexpressed long noncoding RNAs (lncRNAs) in renal tissues of db/db DN mice compared with db/m mice by RNA sequencing. In this study, 5 lincRNAs were confirmed to express in a consistent trend among these DN-related lncRNAs both in vivo and in vitro. Particularly, 1700020I14Rik was the downregulated one. Moreover, our data showed overexpression or knockdown of 1700020I14Rik could regulate cell proliferation and fibrosis in mouse mesangial cells (MCs). Furthermore, 1700020I14Rik was found to interact with miR-34a-5p via both the directly targeting way by bioinformatic investigation and luciferase assay and the Ago2-dependent manner by RIP assay. Results also displayed that overexpression of 1700020I14Rik inhibited cell proliferation and expressions of renal fibrosis markers through miR-34a-5p/Sirt1/HIF-1α pathway in MCs under high glucose condition, while knockdown of 1700020I14Rik could increase cell proliferation and expressions of renal fibrosis markers. In conclusion, these results provide new insights into the regulation between 1700020I14Rik and miR-34a-5p/Sirt1/HIF-1α signaling pathway during the progression of DN.

Indexed as

Cell ProliferationSignal TransductionAnimalsDiabetes Mellitus, ExperimentalDiabetic NephropathiesFibrosisGlomerular MesangiumHypoxia-Inducible Factor 1, alpha SubunitMaleMiceMicroRNAsRNA, Long NoncodingSirtuin 1Hif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitMicroRNAsMIRN34a microRNA, mouseRNA, Long NoncodingSirt1 protein, mouseSirtuin 1

Identifiers

PMID29700282
PMCPMC5919933
OpenAlexW2800240734

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.