Deficiency of ATF3 facilitates both angiotensin II‐induced and spontaneously formed aortic aneurysm and dissection development by activating cGAS–STING pathway

ATF3 deficiency led to degradation of P21 through ubiquitination, which abolished the G1 phase arrest. VSMCs had no time window to repair the damaged DNA, leading to generation of micronuclei in cytoplasm. Cytoplasmic micronuclei facilitating the activation of cGAS-STING pathway, thus inducing the phenotypic switch and apoptosis of VSMCs.