ArticleFrontiers in pharmacology2024
DDIT4/mTOR signaling pathway mediates cantharidin-induced hepatotoxicity and cellular damage.
Article in Frontiers in pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Processing-induced detoxification of toxic Traditional Chinese Medicines: a systematic review of attenuation mechanisms at physical, chemical, and in vivo levels.Chinese medicine · 2026Review
- Effects of hepatic lipid ratio on lipid metabolism indices and hepatic gene expression in late-phase laying hens.Poultry science · 2026Article
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Authors and funding
7 authors.
Funding
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Abstract
Background: Cantharidin (CTD) extracted from the traditional Chinese medicine Methods: In this study, we established models of CTD-induced liver and L-O2 cell damage in mice Results: Following CTD exposure, the mouse liver showed significant pathological damage and an increase in autophagic lysosomes, while the vitality of L-O2 cells showed a significant decrease. CTD led to a significant increase in the mRNA and protein levels of DDIT4 in both liver tissue and L-O2 cells, as well as a significant increase in LC3-II, Beclin1, and Bax, whereas p-mTOR and Bcl-2 were significantly decreased. Following DDIT4 interference and 3-MA treatment, the levels of autophagy and apoptosis induced by CTD in L-O2 cells were reduced. After Rap treatment, both autophagy and apoptosis of CTD-induced L-O2 cells were significantly enhanced. Conclusion: The molecular mechanism of CTD-induced toxicity in mouse liver and L-O2 cells is mainly through DDIT4/mTOR signaling pathway activation, leading to an increase in autophagy and apoptosis levels.
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