ArticleFrontiers in pharmacology2026
Liquiritin restores metabolic homeostasis in NAFLD by modulating AKT1/FOXO1 signaling.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Non-alcoholic fatty liver disease (NAFLD) is a prevalent chronic liver condition with a complex and multifactorial pathogenesis. Purpose: This study aimed to investigate the mecha-nism of liquiritin (LQ) in NAFLD for its treatment. Methods: This study integrates bioinformatics analysis with Results: Bulk RNA-seq analysis identified FOXO1 as a key target, while single-cell analysis predicted interactions between hepatocytes and macrophages in non-alcoholic fatty liver disease (NAFLD). Molecular docking predicted a potential stable interaction between liquiritin and FOXO1. In HepG2 cells and AML12 cells, liquiritin improved NAFLD lipid metabolism disorders by regulating the AKT/FOXO1 pathway. Liquiritin also modulates the expression of mitophagy-associated proteins in RAW264.7 cells. Conclusion: Liquiritin improves lipid metabolism disorders in NAFLD by regulating the AKT/FOXO1 pathway, while also potentially influencing macrophage function. This suggests its potential as a candidate therapeutic agent for non-alcoholic fatty liver disease.
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