Fig. 6
The release of mtDNA induced PANoptosis in VSMCs via activating the cGAS-STING pathway. a, b Western blot assessed the effects of hypoxia treatment on the expressions of cGAS-STING pathway and PANoptosis-related proteins in VSMCs (n = 3 independent experiments). c, d Western blot determined the influence of siArg1 on the expressions of cGAS-STING pathway and PANoptosis-related proteins in VSMCs (n = 3 independent experiments). e, f The influence of the Arg1 E42A mutation on the expressions of cGAS-STING pathway and PANoptosis-related proteins in VSMCs (n = 3 independent experiments). g Flow cytometry was utilized to detect apoptosis in cells (n = 3 independent experiments). h The viability of VSMCs was measured using the CCK-8 assay (n = 6 independent experiments). i, j WB detected the impact of STING agonist on PANoptosis-related proteins in SMAs from ischemic Arg1 KO mice (n = 3 independent experiments). k The vascular reactivity of SMA upon NE stimulation in STING agonist treated ischemic Arg1 KO mice (n = 6 mice in each group). l Variations in SMA diameter reacting to NE concentrations ranging from 10-7 to 10-3 mol/L of ischemic Arg1 KO mice treated with STING agonist (n = 6 mice in each group). m Laser speckle contrast imaging monitored the intestinal blood flow in ischemic Arg1 KO mice treated with STING agonist (bar = 1 cm) (n = 6 mice in each group). a: p < 0.05, as compared with the Normal group; b: p < 0.05, as compared with the Hypoxia + siNC group or Ischemia + Arg1-/- group; c: p < 0.05, as compared with the Hypoxia + Arg1WT group
