T‐2 Toxin‐Mediated β‐Arrestin‐1 O‐GlcNAcylation Exacerbates Glomerular Podocyte Injury via Regulating Histone Acetylation

T‐2 Toxin‐Mediated β‐Arrestin‐1 O‐GlcNAcylation Exacerbates Glomerular Podocyte Injury via Regulating Histone Acetylation

Abstract T‐2 toxin causes renal dysfunction with proteinuria and glomerular podocyte damage. This work explores the role of metabolic disorder/reprogramming‐mediated epigenetic modification in the progression of T‐2 toxin‐stimulated podocyte injury. A metabolomics experiment is performed to assess m...

Full description

Bibliographic Details
Main Authors: Tushuai Li, Wenxue Sun, Shenglong Zhu, Chengsheng He, Tong Chang, Jie Zhang, Yongquan Chen
Format: Article
Language:English
Published: Wiley 2024-02-01
Series:Advanced Science
Subjects:
β‐arrestin‐1
glomerular injury
histone acetylation
o‐glcnacylation
podocyte injury
T‐2 toxins
Online Access:https://doi.org/10.1002/advs.202307648

Internet

https://doi.org/10.1002/advs.202307648

Similar Items