Role of Macrophage Socs3 in the Pathogenesis of Aortic Dissection

Aortic stress caused focal medial rupture that healed in 6 weeks in wild-type mice, but progressed to aortic dissection in mice with macrophage-specific deletion of Socs3.

• Focal medial rupture at the branching point of the celiac trunk and superior mesenteric artery was observed after aortic stress from infrarenal aorta stiffening and angiotensin II infusion.
• Mice lacking the Socs3 gene in macrophages exhibited premature cell proliferation and an inflammatory response linked to the development of aortic dissection.
• Macrophage-specific deletion of Socs3 led to skewed differentiation of macrophages toward a tissue-destructive phenotype.
• Changes in smooth muscle cell behavior and signaling pathways involved in tissue repair were noted in Socs3-deficient mice.
• Activation of signal transduction and activator of transcription 3 was identified in adventitial macrophages in human aortic dissection samples.

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