Methylglyoxal-derived hydroimidazolone-1/RAGE axis induces renal oxidative stress and renal fibrosis in vitro and in vivo.
Toxicology
; 507: 153887, 2024 Sep.
Article
em En
| MEDLINE
| ID: mdl-39019314
ABSTRACT
Advanced glycation end products (AGEs) are important contributors to the progression of chronic kidney diseases (CKD), including renal fibrosis. Although the relationship between AGEs and renal fibrosis has been well studied, the mechanisms of individual AGE-induced renal injury remain poorly understood. This study investigated the adverse effect of methylglyoxal-derived hydroimidazolone-1 (MG-H1), a methylglyoxal (MG)-derived AGE generated by the glycation of MG and arginine residues, on kidney damage. We aimed to elucidate the molecular mechanisms of MG-H1-mediated renal injury and fibrosis, focusing on the receptor for AGEs (RAGE) signaling and its effects on the Wnt/ß-catenin pathway, MAPK pathway, and inflammatory responses. Our results suggest that the MG-H1/RAGE axis plays a significant role in the pathogenesis of CKD and its downstream events involving MAPK kinase-related factors and inflammatory factors. MG-H1 treatment modulated the expression of inflammatory cytokines (TNF-α, IL-6, and IL-1ß) and MAPK proteins (ERK1/2, JNK, and p38).
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Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Aldeído Pirúvico
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Fibrose
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Estresse Oxidativo
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Receptor para Produtos Finais de Glicação Avançada
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Imidazóis
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Rim
Idioma:
En
Ano de publicação:
2024
Tipo de documento:
Article