Role of cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon genes pathway in diabetes and its complications

Table 3 Mechanistic and physiologic effects of stimulator of interferon gene inhibitors associated with diabetes and its complications

Inhibitor	Mechanism	Physiologic effects
Nitro fatty acids	Inhibits palmitoylation by binding to STING[101]	Nitro fatty acids protect against mitochondrial damage in hepatocytes of mice with nonalcoholic fatty liver disease[102]
C-176	Covalent small molecule inhibitors. Inhibits STING palmitoylation[103]	C-176 attenuates cGAS-STING pathway-mediated diabetic cardiomyopathy[54]
UNC93B1	The mechanism of action involves the targeting of STING degradation via the autophagy-lysosome pathway[104]	Unc93b1 ameliorates neuronal apoptosis induced by high glucose through the TLR9 signaling pathway[105]
SP23	Hydrolysis STING by the ubiquitin-proteasome pathway[106]	Improvement of inflammation by decreasing IFN-β release from Th1 cells

cGAS: Cyclic guanosine monophosphate-adenosine monophosphate synthase; STING: Stimulator of interferon gene; IFN: Interferon; Th1: T helper type 1; TLR9: Toll-like receptor 9.