ArticleFrontiers in pharmacology2022
The serum acylcarnitines profile in epileptic children treated with valproic acid and the protective roles of peroxisome proliferator-activated receptor
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Metabolic heterogeneity, networks, and biomarkers of drug-induced liver injury.Journal of pharmaceutical analysis · 2026Article
- Probiotic Limosilactobacillus reuteri DSM 17938 Alleviates Acute Liver Injury by Activating the AMPK Signaling via Gut Microbiota-Derived Propionate.Probiotics and antimicrobial proteins · 2025Article
- Study of acute lethality, teratogenesis, and metabolomic changes of N-(2'-hydroxyphenyl)-2-propylpentanamide (HO-AAVPA) on Artemia franciscana.Scientific reports · 2025Article
- Mechanisms Underlying the Protective Effects of Obeticholic Acid-activated FXR in Valproic Acid-induced HepatotoxicityCurrent computer-aided drug design · 2025Article
- Effect of mitochondrial dysfunction on scar formation after spinal cord injury.Frontiers in neurologyReview
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Authors and funding
6 authors.
Funding
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Abstract
Valproic acid (VPA) is widely used as a major drug in the treatment of epilepsy. Despite the undisputed pharmacological importance and effectiveness of VPA, its potential hepatotoxicity is still a major concern. Being a simple fatty acid, the hepatotoxicity induced by VPA has long been considered to be due primarily to its interference with fatty acid β-oxidation (β-FAO). The aim of this study was to investigate the biomarkers for VPA-induced abnormal liver function in epileptic children and to determine potential mechanisms of its liver injury. Targeted metabolomics analysis of acylcarnitines (ACs) was performed in children's serum. Metabolomic analysis revealed that VPA -induced abnormal liver function resulted in the accumulation of serum long-chain acylcarnitines (LCACs), and the reduced expression of β-FAO relevant genes (Carnitine palmitoyltrans-ferase (CPT)1, CPT2 and Long-chain acyl-CoA dehydrogenase (LCAD)), indicating the disruption of β-FAO. As direct peroxisome proliferator-activated receptor
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