Methylglyoxal induces oxidative stress and ferroptosis of renal tubular epithelial cells in acute and chronic kidney injury mice.

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 m

SUBMITTER: Zhang Y 

PROVIDER: S-EPMC12492953 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature