ArticleAntioxidants (Basel, Switzerland)2022
Glycolaldehyde, an Advanced Glycation End Products Precursor, Induces Apoptosis via ROS-Mediated Mitochondrial Dysfunction in Renal Mesangial Cells.
Article in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Unveiling the role of air pollution in diabetic kidney disease: an integrated study combining network toxicology, machine learning, and Mendelian randomization.Renal failure · 2026Article
- Wen-Shen-Tong-Luo-Zhi-Tong Decoction alleviates bone loss in aged mice by suppressing LONP1-mediated macrophage senescence.Pharmaceutical biology · 2025Article
- Chemoselective Stabilized Triphenylphosphonium Probes for Capturing Reactive Carbonyl Species and Regenerating Covalent Inhibitors with Acrylamide Warheads in Cellulo.Journal of the American Chemical Society · 2025Article
- Association of serum calcium levels with diabetic kidney disease in normocalcemic type 2 diabetes patients: a cross-sectional study.Scientific reports · 2024Article
- Glycation in the cardiomyocyte.Vitamins and hormones · 2024Review
- Organosulfurs, S-allyl cysteine and N-acetyl cysteine sequester di-carbonyls and reduces carbonyl stress in HT22 cells.Scientific reports · 2023Article
- A Role for Advanced Glycation End Products in Molecular Ageing.International journal of molecular sciences · 2023Review
- Diabetic vascular diseases: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2023Review
- N-Acetylcysteine, an ROS Inhibitor, Alleviates the Pathophysiology of Hyperthyroidism-Induced Cardiomyopathy via the ROS/CaBiomolecules · 2022Article
- Structure‒function‒pathogenicity analysis of C-terminal myocilin missense variants based on experiments and 3D models.Frontiers in genetics · 2022Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Glycolaldehyde (GA) is a reducing sugar and a precursor of advanced glycation end products (AGEs). The role of precursor and precursor-derived AGEs in diabetes and its complications have been actively discussed in the literature. This study aimed to elucidate the mechanism of GA-induced apoptosis in renal cells. Immunoblotting results showed that GA (100 μM) caused cytotoxicity in murine renal glomerular mesangial cells (SV40 MES 13) and induced apoptosis via major modulators, decreasing Bcl-2 and increasing Bax, cytochrome c, and cleaved caspase-3/-9 expression. GA-derived AGE accumulation and receptor for AGE (RAGE) expression increased in mesangial cells; however, cells that were cotreated with aminoguanidine (AG) showed no increase in GA-derived AGE concentration. Furthermore, reactive oxygen species (ROS) production was increased by GA, while AG inhibited AGE formation, leading to a decrease in ROS levels in mesangial cells. We evaluated apoptosis through fluorescence-activated cell sorting, and used TUNEL staining to study DNA fragmentation. Additionally, we measured ATP generation and used MitoTracker staining to access changes in mitochondrial membrane potential. This study showed that GA increased AGE concentration, RAGE expression, and excessive ROS generation, leading to renal mesangial cell damage via GA-induced apoptosis pathway caused by mitochondrial dysfunction.
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