ArticleNutrition & metabolism2019
The effect of dicarbonyl stress on the development of kidney dysfunction in metabolic syndrome - a transcriptomic and proteomic approach.
Article in Nutrition & metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Protein glycation products associate with progression of kidney disease and incident cardiovascular events in individuals with type 1 diabetes.Cardiovascular diabetology · 2024Article
- Glyoxalase I is a novel target for the prevention of metabolic derangement.Pharmacology & therapeutics · 2023Review
- Methylglyoxal and Its Adducts: Induction, Repair, and Association with Disease.Chemical research in toxicology · 2022Review
- Article
- Recent Progress in Metabolic Syndrome Research and Therapeutics.International journal of molecular sciences · 2021Review
- Sterol regulatory element-binding protein Sre1 regulates carotenogenesis in the red yeastJournal of lipid research · 2020Article
- Downregulation of theAntioxidants (Basel, Switzerland) · 2020Article
- In vivo AAV delivery of glutathione reductase gene attenuates anti-aging gene klotho deficiency-induced kidney damage.Redox biology · 2020Article
- Adverse Effects of Methylglyoxal on Transcriptome and Metabolic Changes in Visceral Adipose Tissue in a Prediabetic Rat Model.Antioxidants (Basel, Switzerland) · 2020Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimsDicarbonyl stress plays an important role in the pathogenesis of microvascular complications that precede the formation of advanced glycation end products, and contributes to the development of renal dysfunction. In renal cells, toxic metabolites like methylglyoxal lead to mitochondrial dysfunction and protein structure modifications.In our study, we investigated the effect of methylglyoxal on metabolic, transcriptomic, metabolomic and proteomic profiles in the context of the development of kidney impairment in the model of metabolic syndrome. MATERIALS AND
methodsDicarbonyl stress was induced by intragastric administration of methylglyoxal (0.5 mg/kg bw for 4 weeks) in a strain of hereditary hypertriglyceridaemic rats with insulin resistance and fatty liver.
resultsMethylglyoxal administration aggravated glucose intolerance (AUC
conclusionOur results support the hypothesis that dicarbonyl stress plays a key role in renal microvascular complications. At the transcriptome level, methylglyoxal activated oxidative and pro-inflammatory pathways and inhibited angiogenesis. These effects were further supported by the results of urinary proteomic and metabolomic analyses.
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Registered trials
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