Evidence map›Paper›PMID 33850227›Full record

ArticleScientific reports2021

Methylglyoxal induces p53 activation and inhibits mTORC1 in human umbilical vein endothelial cells.

Xinmiao Zhang, Angelica Rodriguez-Niño, Diego O Pastene, Prama Pallavi, Jacob van den Born, Stephan J L Bakker, Bernhard K Krämer, Benito A Yard

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 26 citations in OpenAlex.

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  11. ABCB5Stem cell research & therapy · 2023
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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

8 authors at 5 institutions in 2 countries.

Xinmiao ZhangDepartment of Nephrology, Endocrinology and Rheumatology, Fifth Department of Medicine, University Hospital Mannheim, Heidelberg University, Theodor-Kutzer-Ufer 1-3, 68167, Mannheim, Germany. xinmiaozhang1@outlook.com.
Angelica Rodriguez-NiñoDepartment of Nephrology, Endocrinology and Rheumatology, Fifth Department of Medicine, University Hospital Mannheim, Heidelberg University, Theodor-Kutzer-Ufer 1-3, 68167, Mannheim, Germany.
Diego O PasteneDepartment of Nephrology, Endocrinology and Rheumatology, Fifth Department of Medicine, University Hospital Mannheim, Heidelberg University, Theodor-Kutzer-Ufer 1-3, 68167, Mannheim, Germany.
Prama PallaviSurgical Department, University Hospital Mannheim, Heidelberg University, Mannheim, Germany.
Jacob van den BornDepartment of Internal Medicine, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Stephan J L BakkerDepartment of Internal Medicine, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Bernhard K KrämerDepartment of Nephrology, Endocrinology and Rheumatology, Fifth Department of Medicine, University Hospital Mannheim, Heidelberg University, Theodor-Kutzer-Ufer 1-3, 68167, Mannheim, Germany.
Benito A YardDepartment of Nephrology, Endocrinology and Rheumatology, Fifth Department of Medicine, University Hospital Mannheim, Heidelberg University, Theodor-Kutzer-Ufer 1-3, 68167, Mannheim, Germany.
University Hospital Heidelberg · DEUniversity of Groningen · NLHeidelberg University · DEUniversity Medical Center Groningen · NLUniversity Medical Centre Mannheim · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Methylglyoxal (MGO), a precursor of advanced glycation end products (AGEs), is regarded as a pivotal mediator of vascular damage in patients with diabetes. We have previously reported that MGO induces transcriptional changes compatible with p53 activation in cultured human endothelial cells. To further substantiate this finding and to explore the underlying mechanisms and possible consequences of p53 activation, we aimed (1) to provide direct evidence for p53 activation in MGO-treated human umbilical vein endothelial cells (HUVECs), (2) to assess putative mechanisms by which this occurs, (3) to analyze down-stream effects on mTOR and autophagy pathways, and (4) to assess the potential benefit of carnosine herein. Exposure of HUVECs to 800 µM of MGO for 5 h induced p53 phosphorylation. This was paralleled by an increase in TUNEL and γ-H2AX positive cells, indicative for DNA damage. Compatible with p53 activation, MGO treatment resulted in cell cycle arrest, inhibition of mTORC1 and induction of autophagy. Carnosine co-treatment did not counteract MGO-driven effects. In conclusion, our results demonstrate that MGO elicits DNA damage and p53 activation in HUVECs, resulting in modulation of downstream pathways, e.g. mTORC1.

Indexed as

AutophagyCarnosineCell ShapeCell SurvivalGlycosylationHumansHuman Umbilical Vein Endothelial CellsMechanistic Target of Rapamycin Complex 1Oxidative StressPyruvaldehydeReactive Oxygen SpeciesTumor Suppressor Protein p53CarnosineMechanistic Target of Rapamycin Complex 1PyruvaldehydeReactive Oxygen SpeciesTumor Suppressor Protein p53

Identifiers

PMID33850227
PMCPMC8044125
OpenAlexW3153583846

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.