ArticleInternational journal of molecular sciences2026
Forchlorfenuron Exposure Induces Hepatocyte Apoptosis via MKK3/P38/ATF2 Pathway.
Article in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
- Contribution of p38 MAPK in liver fibrosis: An overview of mechanisms, signaling pathways, and therapeutic targets (Review).International journal of molecular medicine · 2026Review
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Authors and funding
6 authors.
Funding
Abstract
Forchlorfenuron is a widely used plant cytokinin in Traditional Chinese Medicine and agricultural cultivation to boost resistance, postpone senescence, and increase productivity. However, the improper use of forchlorfenuron results in excessive residues and contamination, raising health and safety concerns. Our research investigated the toxicity of forchlorfenuron on hepatocytes in vitro. Results showed that forchlorfenuron inhibited HepaRG cell viability in a concentration and time-dependent manner. Forchlorfenuron-induced cellular apoptosis and the increased intracellular reactive oxygen species (ROS) indicated the participation of oxidative stress. Molecular docking and network pharmacology data suggested that the hepatotoxicity of forchlorfenuron might involve the MAPK signaling pathway. After 24 h of forchlorfenuron exposure, the P38-MAP kinase, upstream kinases MKK3, and the transcription factor ATF2 were maximally activated. Apoptosis induced by forchlorfenuron was significantly reduced by pretreatment with the P38 inhibitor SB203580. These findings implicated that HepaRG hepatocyte injuries were generated by forchlorfenuron through the induction of cellular apoptosis via the MKK3/P38/ATF2 pathway. Forchlorfenuron application should be closely managed to prevent potential liver damage.
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Registered trials
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