Evidence map›Paper›PMID 31257485›Full record

ArticleMolecular medicine reports2019

Betaine alleviates high glucose‑induced mesangial cell proliferation by inhibiting cell proliferation and extracellular matrix deposition via the AKT/ERK1/2/p38 MAPK pathway.

Xianhui Li, Li Wang, Huining Ma

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

10 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
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  5. Molecular medicine reports · 2021
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  6. Observational
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  10. Review
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

3 authors at 3 institutions in 1 country.

Xianhui LiDepartment of Traditional Chinese Medicine, Tianjin Key Laboratory of Artificial Cell, Tianjin Institute of Hepatobiliary Disease, Artificial Cell Engineering Technology Research Center of Public Health Ministry, Third Central Hospital of Tianjin, Tianjin 300170, P.R. China.
Li WangDepartment of Basic Medicine, Tianjin Medical College, Tianjin 300222, P.R. China.
Huining MaDepartment of Traditional Chinese Medicine, Tianjin 4th Centre Hospital, Tianjin 300140, P.R. China.
Tianjin Medical University · CNTianjin Third Central Hospital · CNTianjin University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic nephropathy (DN) is a major cause of chronic renal failure in diabetic patients worldwide. Betaine, a zwitterionic quaternary ammonium salt compound, is involved in numerous biological processes. The present study aimed to investigate the effects of betaine on mouse mesangial cells (MMCs) cultured under high glucose (HG) conditions and its underlying mechanisms. MMCs were treated with betaine under HG conditions. Cell proliferation and the cell cycle distribution were investigated with an MTT assay and flow cytometry, respectively. Western blotting and reverse transcription‑quantitative polymerase chain reaction analyses were applied to respectively determine protein and mRNA expression levels. The results suggested that betaine decreased cell proliferation in a dose‑dependent manner, while G1‑phase arrest was significantly induced in MMCs. Compared with the control group, the expression levels of p21 and p27 decreased under HG conditions, but were reversed by betaine. Furthermore, the expression levels of fibronectin and type IV collagen were significantly decreased in cells treated with betaine compared with the HG group. Additionally, betaine decreased the phosphorylation of Akt, extracellular‑signal‑regulated kinase (Erk)1/2 and p38 mitogen‑activated protein kinase (MAPK), but was enhanced under HG conditions. Overall, the results of the present study indicated that betaine serves a protective role in HG‑induced MMCs by inhibiting cell proliferation and extracellular matrix deposition via regulating regulation of the Akt/Erk1/2/p38 MAPK signaling pathway.

Indexed as

AnimalsBetaineCell ProliferationCells, CulturedDiabetic NephropathiesEnzyme ActivationExtracellular MatrixGlucoseMesangial CellsMiceMitogen-Activated Protein KinasesProto-Oncogene Proteins c-aktSignal TransductionBetaineGlucoseMitogen-Activated Protein KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID31257485
PMCPMC6625408
OpenAlexW2949292848

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.