GALNT4 controls aortic dissection by regulating vascular smooth muscle cell phenotype switch and dysfunction through the TGF-β/smad signaling

GALNT4 expression is significantly elevated in the arteries of human aortic dissection patients and murine models (P < 0.01).

• Knockdown of GALNT4 in smooth muscle cells reduced aortic dissection incidence from 76.9% to 53.8% and rupture rates from 70.0% to 28.6%.
• Higher GALNT4 levels in vascular smooth muscle cells were observed in both human and mouse aortic dissection tissues compared to normal arteries.
• GALNT4 knockdown improved aortic dissection pathology by preserving contractile markers and suppressing synthetic markers in mice.
• In vitro knockdown of GALNT4 inhibited the migration and phenotypic switching of human aortic smooth muscle cells induced by Ang II.
• GALNT4 knockdown reduced a specific type of protein modification on TGF-βR2, which then inhibited the activation of downstream signaling pathways.

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