Figure 1.

The involvement of cGAS-STING, as well as STIM1, in various of steps toward the developments of AS. During the progression of atherosclerosis, overexpression of TMEM203 promotes stored Ca²⁺ depletion, which in turn promotes STIM1 dissociation from STING and its translocation to the cell membrane to bind to Orai1. These lead to elevated intracellular calcium ion concentration and promotion of the atherosclerotic process. On the other hand, elevated intracellular calcium ions lead to direct activation of cGAS-STING, or competitive binding of TMEM203 to STING promotes its dissociation of STIM1 from STING. Activated STING promotes IFN-mediated inflammatory responses. Thus, STIM1 and STING promote lipid deposition, endothelial cell injury, macrophage aggregation, smooth muscle cell proliferation, and phenotypic transformation.