Evidence map›Paper›PMID 29285014›Full record

ArticleEXCLI journal2017

microRNA-503 contribute to pancreatic beta cell dysfunction by targeting the mTOR pathway in gestational diabetes mellitus.

Ke Xu, Dezhi Bian, Lanxiang Hao, Fei Huang, Min Xu, Jie Qin, Yanmei Liu

Open access · greenAbstract read
In one paragraph

Article in EXCLI journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
3.8field-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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. The role of microRNAs in pregnancies complicated by maternal diabetes.Clinical science (London, England : 1979) · 2024
    Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Activation of Rictor/mTORC2 signaling acts as a pivotal strategy to protect against sensorineural hearing loss.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  18. The Mystery of Exosomes in Gestational Diabetes Mellitus.Oxidative medicine and cellular longevity · 2022
    Review
  19. Review
  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

7 authors at 1 institution in 1 country.

Ke XuDepartment of Endocrinology, Yancheng First City Hospital of Jiangsu Province, Yancheng, China.
Dezhi BianDepartment of Endocrinology, Yancheng First City Hospital of Jiangsu Province, Yancheng, China.
Lanxiang HaoDepartment of Endocrinology, Yancheng First City Hospital of Jiangsu Province, Yancheng, China.
Fei HuangDepartment of Endocrinology, Yancheng First City Hospital of Jiangsu Province, Yancheng, China.
Min XuDepartment of Obstetrics and Gynecology, Yancheng First City Hospital of Jiangsu Province, Yancheng, China.
Jie QinDepartment of Pediatrics, Yancheng First City Hospital of Jiangsu Province, Yancheng, China.
Yanmei LiuDepartment of Endocrinology, Yancheng First City Hospital of Jiangsu Province, Yancheng, China.
Nantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Loss of pancreatic β cells is involved in pathogenesis of gestational diabetes mellitus (GDM). Recently, several studies have elucidated the connection between microRNAs (miRNAs) and diabetes mellitus (DM), but the role of miRNAs in GDM remains unclear. The aim of this study was to evaluate the potential functions of miRNAs in GDM and to investigate the underlying mechanisms of action. First, we explored the expression profile of miRNAs in placenta tissue from GDM patients using microarray. Validation analysis was performed in peripheral blood specimens using quantitative reverse transcription PCR (qRT-PCR). Then the role and regulating mechanism of miR-503 in weaken the function of pancreatic β cell was investigated. We found that miR-503 was markedly upregulated in placenta tissue from GDM patients, as elevated in peripheral blood specimens, and the high level was positively correlated to blood glucose concentration. Knockdown of miR-503 enhanced insulin secretion of pancreatic β-cells, promoted cell proliferation and protected cells from apoptosis, whereas overexpression of miR-503 showed the opposite effects. Furthermore, mammalian target of rapamycin (mTOR) was identified as a direct target of miR-503 and mTOR silencing could reverse the improving effects of miR-503 knockdown on insulin secretion and pancreatic β-cells proliferation. High expression of miR-503 in peripheral blood may be acted as a diagnosis biomarker of GDM. MiR-503 regulated functions of pancreatic β-cells by targeting the mTOR pathway, suggesting that targeting miR-503/mTOR axis could serve as a novel therapeutic target for GDM.

Indexed as

gestational diabetes mellitusmicroRNA-503mTORpancreatic beta-cells

Identifiers

PMID29285014
PMCPMC5735340
OpenAlexW3022855430

What OpenQuestion holds

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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.