Fig. 4

Hoxa5 inhibits the cGAS-STING-TBK1-IRF3 pathway and promotes energy metabolism. A iWAT was collected from mice in Chow and HFD groups; immunoblotting analysis was performed on p-TBK1/TBK1 (84 kDa), p-IRF3/IRF3 (57 kDa), and UCP1 (33 kDa). B iWAT was collected from each group of mice after overexpression/interference of Hoxa5; immunoblotting analysis was performed on p-TBK1/TBK1 (84 kDa), p-IRF3/IRF3 (57 kDa), and UCP1 (33 kDa). C iWAT was collected from each group of mice after overexpression/interference of Hoxa5, Pgc1α, Tfam, Nrf1, and Nrf2 were quantified using RT-qPCR. D Mouse primary adipocytes were treated with palmitic acid with the addition of 2', 3'-cGAMP after overexpression/interference of Hoxa5; immunoblotting analysis was performed on STING (46 kDa), p-TBK1/TBK1 (84 kDa), p-IRF3/IRF3 (57 kDa), and UCP1 (33 kDa). E Mouse primary adipocytes were treated with palmitic acid with the addition of C-178 after overexpression/interference of Hoxa5; immunoblotting analysis was performed on STING (46 kDa), p-TBK1/TBK1 (84 kDa), p-IRF3/IRF3 (57 kDa), and UCP1 (33 kDa). F Mouse primary adipocytes were treated with palmitic acid with the addition of C-178 after overexpression/interference of Hoxa5, followed by incubation with the NRF2 antibody, labeling by fluorescent secondary antibody followed by imaging by fluorescence microscopy. G Mouse primary adipocytes were treated with palmitic acid with the addition of 2', 3'-cGAMP after overexpression/interference of Hoxa5; immunoblotting analysis was performed on Nrf2 (66 kDa). H Mouse primary adipocytes were treated with palmitic acid with the addition of  amlexanox after overexpression/interference of Hoxa5; immunoblotting analysis was performed on STING (46 kDa), p-TBK1/TBK1 (84 kDa), p-IRF3/IRF3 (57 kDa), and UCP1 (33 kDa). n = 4 in each group. Values are mean ± SD. *p < 0.05, **p < 0.01. iWAT inguinal white adipose tissue, HFD high fat diet