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.