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deficiency in vascular smooth muscle cells activates a pathogenic CXCL12-CXCR4 signaling axis, which recruits neutrophils and promotes neutrophil extracellular trap formation in aneurysmal tissue. These findings establish a mechanistic link between specific gut microbes, host genetics, and vascular inflammation at single-cell resolution, highlighting promising therapeutic targets for the treatment of aortic aneurysm.
Liu et al. (Fri,) studied this question.