ArticleInflammation2022
TDAG51-Deficiency Podocytes are Protected from High-Glucose-Induced Damage Through Nrf2 Activation via the AKT-GSK-3β Pathway.
Article in Inflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Vestitol Ameliorates Ferroptosis-Associated Features and Osteoarthritis Progression Through Modulation of the GSK3B/Nrf2/GPX4 Pathway.Cell biochemistry and biophysics · 2026Article
- TDAG51 Mediates Negative Signaling Crosstalk Between NGF/p75Neurochemical research · 2025Article
- Glycogen synthase kinase 3β: a key player in progressive chronic kidney disease.Clinical science (London, England : 1979) · 2025Review
- Article
- The potential functions of ferroptosis on urinary stones: mechanisms and therapeutic implications.Frontiers in physiology · 2025Review
- Programmed Cell Death in Diabetic Kidney Disease: Mechanisms and Therapeutic Targeting.Journal of inflammation research · 2025Review
- FGF10 mitigates doxorubicin-induced myocardial toxicity in mice via activation of FGFR2b/PHLDA1/AKT axis.Acta pharmacologica Sinica · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T cell death-associated gene 51 (TDAG51) has been implicated in the development of various pathological conditions. However, whether TDAG51 plays a role in diabetic renal disease remains unknown. The current work investigated the possible function of TDAG51 in diabetic renal disease using high-glucose (HG)-stimulated podocytes in vitro. The elevation of TDAG51 was observed in podocytes in response to HG exposure and the glomeruli of diabetic mice. The siRNAs targeting TDAG51 were applied to deplete TDAG51 in HG-stimulated podocytes. Crucially, TDAG51 deficiency was sufficient to decrease the apoptosis, oxidative stress, and inflammation caused by HG. Mechanically, the inhibition of TDAG51 was capable of enhancing the activation of nuclear factor E2-related factor 2 (Nrf2) associated with the upregulation of AKT-glycogen synthase kinase-3β (GSK-3β) pathway. The reduction of AKT abolished the activation of Nrf2 elicited by TDAG51 deficiency. Additionally, the reduction of Nrf2 diminished the anti-HG injury effect elicited by TDAG51 deficiency. Overall, these data demonstrate that TDAG51 deficiency defends against HG-induced podocyte damage through Nrf2 activation by regulating AKT-GSK-3β pathway. This study suggests that TDAG1 may have a potential role in diabetic renal disease by affecting HG-induced podocyte damage.
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