ArticleBMC cardiovascular disorders2021
Glyoxal damages human aortic endothelial cells by perturbing the glutathione, mitochondrial membrane potential, and mitogen-activated protein kinase pathways.
Article in BMC cardiovascular disorders, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Glyoxal induces arterial injury through the inactivation of receptors and signaling pathways.Molecular and cellular biochemistry · 2026Article
- Formation, Toxicity, and Analytical Techniques for Small-Molecule α-Dicarbonyl Compounds in Foods.Foods (Basel, Switzerland) · 2026Review
- Role of Advanced Glycation End Products and Mitohormesis in Cancer Development and Progression.Antioxidants (Basel, Switzerland) · 2025Review
- Effect of Glyoxal on Plasma Membrane and Cytosolic Proteins of Erythrocytes.International journal of molecular sciences · 2025Article
- Mechanisms of Acetaldehyde-Induced Organ Injury via Impairment of Vascular Endothelial Cells.Vascular health and risk management · 2025Review
- Glyoxal in hyperglycaemic ischemic stroke - a cohort study.Cardiovascular diabetology · 2023Article
- Proteomics-based evaluation of the mechanism underlying vascular injury via DNA interstrand crosslinks, glutathione perturbation, mitogen-activated protein kinase, and Wnt and ErbB signaling pathways induced by crotonaldehyde.Clinical proteomics · 2022Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundExposure to glyoxal, the smallest dialdehyde, is associated with several diseases; humans are routinely exposed to glyoxal because of its ubiquitous presence in foods and the environment. The aim of this study was to examine the damage caused by glyoxal in human aortic endothelial cells.
methodsCell survival assays and quantitative fluorescence assays were performed to measure DNA damage; oxidative stress was detected by colorimetric assays and quantitative fluorescence, and the mitogen-activated protein kinase pathways were assessed using western blotting.
resultsExposure to glyoxal was found to be linked to abnormal glutathione activity, the collapse of mitochondrial membrane potential, and the activation of mitogen-activated protein kinase pathways. However, DNA damage and thioredoxin oxidation were not induced by dialdehydes.
conclusionsIntracellular glutathione, members of the mitogen-activated protein kinase pathways, and the mitochondrial membrane potential are all critical targets of glyoxal. These findings provide novel insights into the molecular mechanisms perturbed by glyoxal, and may facilitate the development of new therapeutics and diagnostic markers for cardiovascular diseases.
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