Metformin attenuates valproic acid–induced developmental cardiotoxicity through activation of the AMPK/PGC-1α axis and restoration of mitochondrial and redox homeostasis in zebrafish embryos

, mitochondrial, and antioxidant capacity by MET suggests that the AMPK/PGC-1α axis may serve as a central target in VPA cardiotoxicity.

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Publication Details

Journal
Drug and Chemical Toxicology
Published
2026-06-08
DOI
https://doi.org/10.1080/01480545.2026.2684476
Primary Topic
Metabolism, Diabetes, and Cancer
Type
article
Field-Weighted Citation Impact
0.00
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article

Metformin attenuates valproic acid–induced developmental cardiotoxicity through activation of the AMPK/PGC-1α axis and restoration of mitochondrial and redox homeostasis in zebrafish embryos

Ünsal Veli Üstündağ, Fümet Duygu Üstündağ, Neşe Ayşit
Drug and Chemical Toxicology
Metabolism, Diabetes, and Cancer
article

Metformin attenuates valproic acid–induced developmental cardiotoxicity through activation of the AMPK/PGC-1α axis and restoration of mitochondrial and redox homeostasis in zebrafish embryos

Ünsal Veli Üstündağ, Fümet Duygu Üstündağ, Neşe Ayşit
article en

Abstract

, mitochondrial, and antioxidant capacity by MET suggests that the AMPK/PGC-1α axis may serve as a central target in VPA cardiotoxicity.

Drug and Chemical Toxicology
Ağrı İbrahim Çeçen University (TR), Istanbul Medipol University (TR)
Life in Land
Openalex Percentile: Top 9%
Metabolism, Diabetes, and Cancer
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