ArticleHeliyon2024
A novel GSK3β inhibitor 5n attenuates acute kidney injury.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 0 citations in OpenAlex.
- Ligustroflavone protects against acute kidney injury by inhibiting ferroptosis via acting on GSK3β/NRF2 signaling.International journal of molecular medicine · 2026Article
- Cinnamaldehyde attenuates LPS-induced acute kidney injury by inhibiting ferroptosis via the Gsk3β/Nrf2/Gpx4 pathway.American journal of translational research · 2026Article
- Glycogen synthase kinase 3β: a key player in progressive chronic kidney disease.Clinical science (London, England : 1979) · 2025Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) is a clinical syndrome with high morbidity and mortality caused by various factor. The specific strategies for AKI are still lacking. GSK3β is widely expressed in the kidneys. In acute models of injury, GSK3β promotes the systemic inflammatory response, increases the proinflammatory release of cytokines, induces apoptosis, and alters cell proliferation. We screened a series of 3-(4-pyridyl)-5-(4-sulfamido-phenyl)-1,2,4-oxadiazole derivatives which are recognized as new GSK3β inhibitors, and found that 5n had the least toxicity and the best cell protection. We then tested the anti-inflammatory and reno-protective effect of 5n in cisplatin-treated tubular epithelial cells. 5n had anti-inflammation effect indicated by phosphor-NF-κB detection. Finally, we found that 5n ameliorated renal injury and inflammation in cisplatin-induced AKI mouse model. Silencing GSK3β inhibited cell injury and inflammation induced by cisplatin. We found that GSK3β interacted with PP2Ac to modulate the activity of NF-κB. In conclusion, 5n, the novel GSK3β inhibitor, protects against AKI via PP2Ac-dependent mechanisms which may provide a potential strategy for the treatment of AKI in clinic.
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Registered trials
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