Editing Cantharidin (section)

===Mechanism of action===
{{missing information|section|toxicological mechanism when ingested|date=September 2022}}
Topical cantharidin is absorbed by the lipid membranes of [[Epidermis|epidermal cells]], causing the release of [[serine proteases]], [[enzymes]] that break the [[peptide bonds]] in proteins. This causes the disintegration of [[Desmosome|desmosomal plaques]], cellular structures involved in cell-to-cell adhesion, leading to detachment of the [[Tonofibril|tonofilaments]] that hold cells together. The process leads to the loss of cellular connections ([[acantholysis]]), and ultimately results in blistering of the skin. Lesions heal without scarring.<ref name=Moed2001>{{cite journal | vauthors = Moed L, Shwayder TA, Chang MW | title = Cantharidin revisited: a blistering defense of an ancient medicine | journal = Archives of Dermatology | volume = 137 | issue = 10 | pages = 1357–1360 | date = October 2001 | pmid = 11594862 | doi = 10.1001/archderm.137.10.1357 | doi-access = free }}</ref><ref name=Bertaux1988>{{cite journal | vauthors = Bertaux B, Prost C, Heslan M, Dubertret L | title = Cantharide acantholysis: endogenous protease activation leading to desmosomal plaque dissolution | journal = The British Journal of Dermatology | volume = 118 | issue = 2 | pages = 157–165 | date = February 1988 | pmid = 3279999 | doi = 10.1111/j.1365-2133.1988.tb01769.x | s2cid = 45714898 }}</ref>