ArticleDrug design, development and therapy2025
Quantitative Proteomic Study Reveals Amygdalin Alleviates Liver Fibrosis Through Inhibiting mTOR/PDCD4/JNK Pathway in Hepatic Stellate Cells.
Article in Drug design, development and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed.
- From diet to disease modulation: the multi-targeted effects of medicinal-food homologous plants in hepatic fibrosis.Frontiers in nutrition · 2026Review
- The Therapeutic Effects of Active Components from Food-Medicine Plants on Liver Fibrosis.Journal of inflammation research · 2026Review
- Effect and Mechanisms of Yiqi Jianpi Xiaoyu Prescription on Kidney Fibrosis on the Basis of Metabolomics and Experimental Validation.Food science & nutrition · 2025Article
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Authors and funding
9 authors.
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Abstract
Purpose: Hepatic fibrosis is a major cause of morbidity and mortality for which there is currently limited therapy. Amygdalin, a cyanogenic glucoside derived from Semen Persicae, exerts significant anti-fibrotic effects in the liver. However, the molecular mechanism by which amygdalin inhibits the progression of liver fibrosis remains unclear. This study aimed to elucidate the potential mechanism of action of amygdalin against liver fibrosis. Methods: Quantitative proteomic profiling of the mouse liver tissues from control, carbon tetrachloride (CCl Results: Amygdalin could effectively ameliorated CCl Conclusion: Our data demonstrated a potential pharmaceutical mechanism by which amygdalin alleviates liver fibrosis by inhibiting the mTOR/PDCD4/JNK pathway in HSCs, suggesting that PDCD4 is a potential target for the treatment of liver fibrosis.
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