What question did this study set out to answer?

To review the molecular and cellular mechanisms through which glycogen synthase kinase 3β (GSK3β) drives chronic kidney disease progression and evaluate its potential as a therapeutic target.

June 1, 2025Clinical ScienceOpen Access

Glycogen synthase kinase 3β: a key player in progressive chronic kidney disease

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Authors

MZMingzhuo Zhang MTMarc Tatar RGRujun Gong

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Overview

Literature review demonstrates GSK3β hyperactivity drives renal fibrosis and damage in chronic kidney disease, suggesting its viability as a therapeutic target.

Key Points

To review the molecular and cellular mechanisms through which glycogen synthase kinase 3β (GSK3β) drives chronic kidney disease progression and evaluate its potential as a therapeutic target.
Narrative synthesis of preclinical and mechanistic studies investigating GSK3β regulation across renal podocytes, mesangial cells, and tubular epithelial cells.
Analysis of signaling pathways modulated by GSK3β, including Wnt/β-catenin, NF-κB, Nrf2, and PI3K/Akt, in the context of progressive renal injury.
GSK3β is overexpressed and hyperactive in chronic kidney disease, driving podocyte injury, mesangial expansion, interstitial fibrosis, and tubular atrophy.
Sustained GSK3β activation maintains profibrotic signaling and oxidative stress in tubular cells, accelerating the transition from acute kidney injury to chronic disease.
Pharmacological inhibition using selective GSK3β inhibitors reduces kidney injury, attenuates renal fibrosis, and promotes functional tissue recovery in preclinical models.

Cite This Study

Zhang et al. (2025) studied this question.

synapsesocial.com/papers/6a162811512cb4f7828e8ccb https://doi.org/10.1042/cs20245219

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June 1, 2025Clinical ScienceOpen Access

Glycogen synthase kinase 3β: a key player in progressive chronic kidney disease

View Full Paper

Ask AI

Bookmark

Authors

MZMingzhuo Zhang MTMarc Tatar RGRujun Gong

Discussion

Member takes

Overview

Literature review demonstrates GSK3β hyperactivity drives renal fibrosis and damage in chronic kidney disease, suggesting its viability as a therapeutic target.

Key Points

To review the molecular and cellular mechanisms through which glycogen synthase kinase 3β (GSK3β) drives chronic kidney disease progression and evaluate its potential as a therapeutic target.
Narrative synthesis of preclinical and mechanistic studies investigating GSK3β regulation across renal podocytes, mesangial cells, and tubular epithelial cells.
Analysis of signaling pathways modulated by GSK3β, including Wnt/β-catenin, NF-κB, Nrf2, and PI3K/Akt, in the context of progressive renal injury.
GSK3β is overexpressed and hyperactive in chronic kidney disease, driving podocyte injury, mesangial expansion, interstitial fibrosis, and tubular atrophy.
Sustained GSK3β activation maintains profibrotic signaling and oxidative stress in tubular cells, accelerating the transition from acute kidney injury to chronic disease.
Pharmacological inhibition using selective GSK3β inhibitors reduces kidney injury, attenuates renal fibrosis, and promotes functional tissue recovery in preclinical models.

Cite This Study

Zhang et al. (2025) studied this question.

synapsesocial.com/papers/6a162811512cb4f7828e8ccb https://doi.org/10.1042/cs20245219

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