ArticlePloS one2026
Artemether ameliorates type 1 diabetic liver injury alongside the associated defects in mitochondrial ultrastructure and central carbon metabolism.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Research Progress on Anti-Inflammatory and Antioxidant Mechanism of Artemether Based on MAPK/NF-κB Signaling Pathway.International journal of molecular sciences · 2026Review
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Authors and funding
9 authors.
Funding
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Abstract
Type 1 diabetes mellitus (T1DM) is characterized by autoimmune-mediated destruction of pancreatic islet β-cells and the resultant absolute insulin deficiency, which leads to systemic metabolic dysregulation. Hepatic injury has emerged as a clinically significant complication of T1DM; however, no targeted therapeutic intervention is currently available. Artemether (Art), a methyl ether derivative of artemisinin, has shown potential in ameliorating hyperglycemia, but its efficacy in mitigating T1DM-associated hepatic dysfunction remains insufficiently elucidated. This study comprehensively evaluates the hepatoprotective effects of Art in a murine model of T1DM, with particular emphasis on mitochondrial structural integrity and the regulation of glucose and lipid metabolism. Hepatic function was assessed through histopathological evaluation, ultrastructural examination of mitochondria via transmission electron microscopy, and molecular analysis of gene and protein expression levels. Metabolic intermediates associated with glucose and lipid metabolic pathways were quantitatively analyzed using ultra-high-performance liquid chromatography coupled with triple quadrupole tandem mass spectrometry (UPLC-QQQ-MS/MS). Administration of Art significantly attenuated both diabetic manifestations and liver injury. Importantly, Art preserved mitochondrial morphology, restored the expression of some proteins related to the respiratory chain complex, and downregulated indicators of hepatic fatty acid β-oxidation, upregulated markers of de novo fatty acid synthesis, normalized intrahepatic triglyceride concentrations, and reduced expression of key molecules involved in gluconeogenesis and glycogenolysis. These findings indicate that Art confers protective effects against liver injury in T1DM through coordinated modulation of mitochondrial function and key metabolic pathways at transcriptional, translational, and metabolic intermediate levels.
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