Evidence map›Paper›PMID 34097717›Full record

ArticlePloS one2021

LncRNA TUG1/miR-29c-3p/SIRT1 axis regulates endoplasmic reticulum stress-mediated renal epithelial cells injury in diabetic nephropathy model in vitro.

Shaoqiang Wang, Pengfei Yi, Na Wang, Min Song, Wenhui Li, Yingying Zheng

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  7. lncRNA TUG1 and kidney diseases.BMC nephrology · 2025
    Review
  8. Review
  9. The role of SIRT1 in kidney diseases.International urology and nephrology · 2025
    Review
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  11. Review
  12. Article
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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 1 institution in 1 country.

Shaoqiang WangDepartment of Thoracic Surgery, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining city, Shandong Province, P.R.China.
Pengfei YiDepartment of Endocrinology, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining city, Shandong Province, P.R.China.
Na WangDepartment of Endocrinology, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining city, Shandong Province, P.R.China.
Min SongDepartment of Endocrinology, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining city, Shandong Province, P.R.China.
Wenhui LiDepartment of Thoracic Surgery, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining city, Shandong Province, P.R.China.
Yingying ZhengDepartment of Endocrinology, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining city, Shandong Province, P.R.China.ORCID 0000-0002-5684-6430
Affiliated Hospital of Jining Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding RNAs (lncRNAs) are important regulators in diabetic nephropathy. In this study, we investigated the potential role of lncRNA TUG1 in regulating endoplasmic reticulum stress (ERS)-mediated apoptosis in high glucose induced renal tubular epithelial cells. Human renal tubular epithelial cell line HK-2 was challenged with high glucose following transfection with lncRNA TUG1, miR-29c-3p mimics or inhibitor expression plasmid, either alone or in combination, for different experimental purposes. Potential binding effects between TUG1 and miR-29c-3p, as well as between miR-29c-3p and SIRT1 were verified. High glucose induced apoptosis and ERS in HK-2 cells, and significantly decreased TUG1 expression. Overexpressed TUG1 could prevent high glucose-induced apoptosis and alleviated ERS via negatively regulating miR-29c-3p. In contrast, miR-29c-3p increased HK-2 cells apoptosis and ERS upon high glucose-challenge. SIRT1 was a direct target gene of miR-29c-3p in HK-2 cells, which participated in the effects of miR-29c-3p on HK-2 cells. Mechanistically, TUG1 suppressed the expression of miR-29c-3p, thus counteracting its function in downregulating the level of SIRT1. TUG1 regulates miR-29c-3p/SIRT1 and subsequent ERS to relieve high glucose induced renal epithelial cells injury, and suggests a potential role for TUG1 as a promising diagnostic marker of diabetic nephropathy.

Indexed as

Endoplasmic Reticulum StressApoptosisCell LineDiabetic NephropathiesEpithelial CellsGlucoseHumansKidneyMicroRNAsRNA, Long NoncodingSirtuin 1GlucoseMicroRNAsMIRN29C microRNA, humanRNA, Long NoncodingSIRT1 protein, humanSirtuin 1TUG1 long noncoding RNA, human

Identifiers

PMID34097717
PMCPMC8183992
OpenAlexW3167583812

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.