CAV1 and inflammatory bowel disease: Both miraculin and mogroside V upregulated tight junction genes (CLDN2, CLDN3, CLDN7, CLDN10) and gap junction genes (GJA1, GJA3, GJA4, GJA5), whilst also modulating adhesion-associated genes, CAV1, ITGB3, DLL1, and DSG3. Notably, CLDN2 induction, as seen with miraculin and mogroside V, is a hallmark of leaky epithelia, frequently observed in inflammatory bowel disease (IBD), where it increases paracellular cation permeability and undermines barrier tightness28.