Figure 3.

The protective mechanism of Zn²⁺ on respiratory diseases. Zn²⁺ can enter airway epithelial cells via ZIP. (A) PDE is responsible for catalyzing the degradation of cGMP and cAMP. Reduced cGMP and cAMP lead to reduced PKA activation, which in turn promotes downstream inflammatory cascades and increased TNF-α expression. Combination of Zn²⁺ and PDE can inhibit the enzyme activity, which reduces the cell damage caused by inflammation. (B) Exogenous apoptosis is mediated by FasL and Fas, while endogenous apoptosis is mediated by mitochondria. Both pathways activate initiator and executioner caspases to promote apoptosis. Zn²⁺ protects the airway epithelium by inhibiting caspase activity to prevent excessive cell death. ZIP, Zrt- and Irt-like protein; PDE, phosphodiesterase; FasL, Fas ligand; Fas, tumor necrosis factor receptor superfamily member 6; FADD, Fas-associated death domain; PKA, protein kinase A; NF-Kb, nuclear transcription factor-kappa B.