ArticleFrontiers in cell and developmental biology2025
Methylglyoxal induces oxidative stress and ferroptosis of renal tubular epithelial cells in acute and chronic kidney injury mice.
Article in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Article
- GLO1 cg26053840 Methylation Associates with Kidney Injury and Inflammatory Markers in Hospitalized Older Adults.Life (Basel, Switzerland) · 2026Article
- Reactive carbonyl species in health and chronic disease: from methylglyoxal to an integrative network of metabolic regulation.Cardiovascular diabetology · 2026Review
- Epithelial redox stress programs macrophage immunometabolism through a ZNF24-MIF-NF-κB pathway in chronic nonbacterial prostatitis.Redox biology · 2026Article
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6 authors.
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Abstract
Methylglyoxal (MG), which is a highly reactive dicarbonyl compound, has been increasingly recognized due to its role in the pathogenesis of kidney injury, particularly in diseases such as diabetic nephropathy and hypertensive nephropathy. MG promotes advanced glycation end product (AGE) formation and directly impairs cell function. MG levels are significantly increased in various renal diseases. This study aimed to investigate the relationship between MG and ferroptosis, which is a form of cell death involving iron-dependent lipid peroxidation (LPO), during kidney injury. Animal and cellular experiments were conducted to verify that ferroptosis occurred after MG treatment, and RNA sequencing (RNA-Seq) was performed to analyse changes in gene expression profiles after MG exposure. A mouse model that mimicked human kidney injury was established by administering folic acid, and the MG and D-lactate levels in serum and tissues were measured.
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