Editing Cantharidin (section)

===Toxicity===
The [[liver]], primarily responsible for metabolism and detoxification, often becomes damaged in cases of cantharidin poisoning. The [[hepatotoxicity]] of cantharidin arises from its inhibition of hepatocyte proliferation pathways, the promotion of hepatocyte [[apoptosis]] or [[autophagy]], and increased inflammation. <ref name="Jin_2023">{{cite journal | vauthors = Jin D, Huang NN, Wei JX | title = Hepatotoxic mechanism of cantharidin: insights and strategies for therapeutic intervention | journal = Frontiers in Pharmacology | volume = 14 | pages = 1201404 | date = 13 June 2023 | pmid = 37383714 | pmc = 10293652 | doi = 10.3389/fphar.2023.1201404 | doi-access = free }}</ref> Many studies have been conducted to elucidate the specific interactions cantharidin has in the liver, that lead to pathology. The poison has been found to inhibit PP1, PP2A (PP = [[protein phosphatase]]), TIL-4 (TIL = [[toll-like receptor]]), NF-KB (NF = [[nuclear factor]]), ERK, and DFF45. Cantharidin promotes TNF-α (TNF = tumor necrosis factor), FASL, ROS, caspase-4, caspase-6, caspase-8, caspase-9, caspase-12, protein kinase R-like ER kinase, inositol-requiring enzyme 1, ATF6 (transcription factor 6), ATF4, BID,BAK, BAX, cyto C, LC3-1, p150, Atg7, P13K Ⅲ, eIF2α, and CHOP pathways.<ref name="Jin_2023" /> Cantharidin has an diverse range of targets in the liver that have been discovered empirically. However, the exact chemical mechanisms by which cantharidin interferes with these structures are unknown.