The main findings of our study are as follows: (1) MT1 expression was significantly elevated and correlated with NET formation in both human and murine AAA tissues; (2) glycoRNA modification markedly enhanced the accumulation of anti-NETs NPs at AAA lesions; (3) GlycoRNA-NP-siMT1 administration attenuated aortic dilatation and reduced the incidence of rupture in a PPE-induced murine AAA model; and (4) GlycoRNA-NP-siMT1 inhibited excessive NET accumulation at AAA lesions through a dual mechanism involving the reduction of neutrophil infiltration and the inhibition of the NETosis process. The gene discussed is MT1A; the disease is triple-A syndrome.