Nafamostat Mesylate Regulates Glycosylation to Alleviate Aristolochic Acid Induced Kidney Injury DOI Creative Commons

Pei Xie,

Huijun Liu,

Xingli Huo

et al.

Toxins, Journal Year: 2025, Volume and Issue: 17(3), P. 145 - 145

Published: March 18, 2025

Acute kidney injury (AKI) is a condition with poor prognosis, exacerbated by the lack of effective therapeutic options and inadequately understood underlying mechanisms. Glycosylation, post-translational modification proteins, essential for maintaining protein stability function, its dysregulation leads to misfolding amyloid aggregation. Glycosylation dynamics are implicated in several pathologies, including inflammation, cancer, AKI, highlighting potential regulating glycosylation preventing aggregation AKI treatment. This study investigates effect nafamostat mesylate (NM) on vivo. Using optical spectroscopy other analytical techniques, we demonstrate that NM restores levels inhibits aristolochic-acid-induced acute injury. The mechanism likely involves enzymatic modulation corrects hypoglycosylation prevents aggregation, promoting proper folding enhancing stability. These findings suggest may provide novel strategy glycosylation-related diseases, underscoring early intervention treatment these conditions.

Language: Английский

Nafamostat Mesylate Regulates Glycosylation to Alleviate Aristolochic Acid Induced Kidney Injury DOI Creative Commons

Pei Xie,

Huijun Liu,

Xingli Huo

et al.

Toxins, Journal Year: 2025, Volume and Issue: 17(3), P. 145 - 145

Published: March 18, 2025

Acute kidney injury (AKI) is a condition with poor prognosis, exacerbated by the lack of effective therapeutic options and inadequately understood underlying mechanisms. Glycosylation, post-translational modification proteins, essential for maintaining protein stability function, its dysregulation leads to misfolding amyloid aggregation. Glycosylation dynamics are implicated in several pathologies, including inflammation, cancer, AKI, highlighting potential regulating glycosylation preventing aggregation AKI treatment. This study investigates effect nafamostat mesylate (NM) on vivo. Using optical spectroscopy other analytical techniques, we demonstrate that NM restores levels inhibits aristolochic-acid-induced acute injury. The mechanism likely involves enzymatic modulation corrects hypoglycosylation prevents aggregation, promoting proper folding enhancing stability. These findings suggest may provide novel strategy glycosylation-related diseases, underscoring early intervention treatment these conditions.

Language: Английский

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