Evidence map›Paper›PMID 35139912›Full record

ArticleDiabetology & metabolic syndrome2022

Trigonelline reverses high glucose-induced proliferation, fibrosis of mesangial cells via modulation of Wnt signaling pathway.

Chen Chen, Yan Shi, Jiulong Ma, Zhen Chen, Ming Zhang, Yan Zhao

Open access · goldAbstract read
In one paragraph

Article in Diabetology & metabolic syndrome, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

11 citing papers in PubMed, 32 citations in OpenAlex.

  1. Wnt/β-Catenin Signaling in Diabetic Complications: Mechanisms and Therapeutic Potential.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026
    Review
  2. Article
  3. Food science & nutrition · 2024
    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 2 institutions in 1 country.

Chen ChenCollege of Pharmacy, Jilin University, Xinmin Street No. 1163, Changchun, People's Republic of China.
Yan ShiCollege of Pharmacy, Jilin University, Xinmin Street No. 1163, Changchun, People's Republic of China.
Jiulong MaCollege of Pharmacy, Jilin University, Xinmin Street No. 1163, Changchun, People's Republic of China.
Zhen ChenCollege of Pharmacy, Jilin University, Xinmin Street No. 1163, Changchun, People's Republic of China.
Ming ZhangCollege of Pharmacy, Jilin University, Xinmin Street No. 1163, Changchun, People's Republic of China.
Yan ZhaoPhysical Examination Center, Jilin University Second Hospital, Street No. 218, Changchun, Ziqiang, People's Republic of China. 790618540@qq.com.ORCID http://orcid.org/0000-0003-0569-5350
Jilin University · CNSecond Affiliated Hospital of Jilin University · CN

Funding

Department of Science and Technology of Jilin Province No. 20210101378JC
6 · The paper itself

Abstract

backgroundDiabetic nephropathy (DN) is the leading cause of the end-stage renal disease (ESRD). The proliferation and apoptosis of mesangial cells induced by the activated Wnt/β-catenin pathway is crucial in DN. Trigonelline (TRL) is an alkaloid that has been shown to decrease proteinuria and protect the renal function in DN. However, the effect of TRL on the Wnt/β-catenin pathway of mesangial cells is unclear.

methodsAs a cellular DN model, human mesangial cells (HMCs) were treated with high-glucose (HG). β-Catenin plasmid and control knockdown plasmids were transfected into HG-treated HMCs as β-catenin pcDNA and β-catenin siRNA groups, respectively. Cell viability was measured by MTT assay. Flow cytometry was used to detect the cell cycle. Cell apoptosis was evaluated by flow cytometry and terminal dUTP transferase nick end labeling (TUNEL) assay. mRNA expression of Wnt1, Wnt3a, Wnt4, Wnt5a, β-catenin, TCF4, Cyclin D1, and CDK4 were detected by qRT-PCR. Protein expression of Wnt4, Wnt5a, nucleus-β-catenin, TCF4, Cyclin D1, and CDK4 were detected by western blotting.

resultsTRL significantly inhibited HG-induced HMCs viability over three-time points measured (24, 48, and 72 h). In addition, TRL suppressed the levels of fibronectin (FN) and collagen IV (Col IV) in HG-stimulated HMCs. Furthermore, TRL efficiently inhibited the activation of the Wnt/β-catenin signaling pathway in HG-stimulated HMCs. Taken together, these data indicated that TRL inhibited HG-induced HMCs proliferation and ECM expression via the modulation of the Wnt signaling pathway.

conclusionsTRL reduces HG-induced cell injury by regulating the Wnt/β-catenin signaling pathway.

Indexed as

ApoptosisDiabetic nephropathyMesangial cellsTrigonellineWnt/β-catenin

Identifiers

PMID35139912
PMCPMC8827266
OpenAlexW4210907062

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.