Evidence map›Paper›PMID 32467587›Full record

ArticleCell death & disease2020

Molecular mechanisms of methylglyoxal-induced aortic endothelial dysfunction in human vascular endothelial cells.

Jae Hyuk Lee, Amna Parveen, Moon Ho Do, Min Cheol Kang, Silvia Yumnam, Sun Yeou Kim

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

40 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Review
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  4. Antioxidants (Basel, Switzerland) · 2026
    Article
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  6. Review
  7. Article
  8. Article
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  16. Food science & nutrition · 2024
    Article
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  18. 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.

Jae Hyuk LeeCollege of Pharmacy, Gachon University, #191, Hambakmoero, Yeonsu-Gu, Incheon, 21936, Republic of Korea.ORCID http://orcid.org/0000-0002-4304-0198
Amna ParveenCollege of Pharmacy, Gachon University, #191, Hambakmoero, Yeonsu-Gu, Incheon, 21936, Republic of Korea.
Moon Ho DoCollege of Pharmacy, Gachon University, #191, Hambakmoero, Yeonsu-Gu, Incheon, 21936, Republic of Korea.
Min Cheol KangCollege of Pharmacy, Gachon University, #191, Hambakmoero, Yeonsu-Gu, Incheon, 21936, Republic of Korea.
Silvia YumnamCollege of Pharmacy, Gachon University, #191, Hambakmoero, Yeonsu-Gu, Incheon, 21936, Republic of Korea.
Sun Yeou KimCollege of Pharmacy, Gachon University, #191, Hambakmoero, Yeonsu-Gu, Incheon, 21936, Republic of Korea. sunnykim@gachon.ac.kr.
Gachon University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Methylglyoxal (MGO)-induced cellular apoptosis, oxidative stress, inflammation, and AGE formation are specific events that induce vascular endothelial cell (EC) toxicity in endothelial dysfunction (ED). MGO accumulates quickly in various tissues and plays a prominent role in the pathogeneses of several diabetic complications. Unbalanced angiogenesis is a gateway to the development of diabetic complications. EC apoptosis and autophagy work together to regulate angiogenesis by interacting with different angiogenic factors. In addition to understanding the deep mechanism regarding MGO-dependent autophagy/apoptosis may provide new therapeutic applications to treat diabetes and diabetic complications. Therefore, the present study aimed to investigate the regulatory effects of MGO-induced autophagy and apoptosis on angiogenesis in HAoEC and to elucidate the molecular mechanisms to discover new target base therapy for diabetes and diabetic complications. In MGO-stimulated HAoEC, protein expression was identified using a western blot, autophagosomes were observed by bio-transmission electron microscopy (TEM), and cell autophagic vacuoles and flux were measured using a confocal microscope. We found that MGO significantly induced autophagy, declined the pro-angiogenic effect, decreased proliferation, migration, and formation of tube-like structures, and increased autophagic vacuoles, flux and autophagosomes in the HAoEC in a dose-dependent manner. We observed that MGO-induced autophagic cell death and inhibited the ROS-mediated Akt/mTOR signaling pathway. MGO also triggered apoptosis by elevating the cleaved caspase-3 to Bax/Bcl-2 ratio and through activation of the ROS-mediated MAPKs (p-JNK, p-p38, and p-ERK) signaling pathway. Collectively, these findings suggest that autophagy and apoptosis inhibit angiogenesis via the ROS-mediated Akt/mTOR and MAPKs signaling pathways, respectively, when HAoEC are treated with MGO.

Indexed as

AortaApoptosisAutophagosomesAutophagybcl-2-Associated X ProteinCaspase 3Cell MovementCell ProliferationCells, CulturedCell SurvivalCytoskeletal ProteinsEndothelial CellsGuanidinesHumansMAP Kinase Signaling SystemMicrotubule-Associated Proteinsbcl-2-Associated X ProteinBCL2 protein, humanCaspase 3Cytoskeletal ProteinsGuanidinesMAP1LC3A protein, humanMicrotubule-Associated ProteinsPhosphatidylinositol 3-KinasespimagedineProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2PyruvaldehydeReactive Oxygen SpeciesTOR Serine-Threonine Kinases

Identifiers

PMID32467587
PMCPMC7256048
OpenAlexW3031684227

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.