The redox-sensitive GSK3β is a key regulator of glomerular podocyte injury in type 2 diabetic kidney disease.
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ABSTRACT: Emerging evidence suggests that GSK3β, a redox-sensitive transducer downstream of insulin signaling, acts as a convergent point for myriad pathways implicated in kidney injury, repair, and regeneration. However, its role in diabetic kidney disease remains controversial. In cultured glomerular podocytes, exposure to a milieu of type 2 diabetes elicited prominent signs of podocyte injury and degeneration, marked by loss of homeostatic marker proteins like synaptopodin, actin cytoskeleton disruption, oxidative stress, apoptosis, and stress-induced premature senescence, as shown by increased staining for senescence-associated β-galactosidase activity, amplified formation of γH2AX foci, and elevated expression of mediators of senescence signaling, like p21 and p16INK4A. These degener
SUBMITTER: Chen M
PROVIDER: S-EPMC10979123 | biostudies-literature | 2024 Mar
REPOSITORIES: biostudies-literature
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