MicroRNA-21 Knockout Exacerbates Angiotensin II–Induced Thoracic Aortic Aneurysm and Dissection in Mice With Abnormal Transforming Growth Factor-β–SMAD3 Signaling

Angiotensin II infusion led to aortic rupture within 23 days in a mouse model of thoracic aortic aneurysm and dissection.

• Dysfunctional TGF-β signaling in vascular smooth muscle cells was linked to the exacerbation of TAAD in specific mouse models.
• Higher levels of phosphorylated ERK and JNK were observed in the lesions associated with TAAD.
• The absence of TGF-β signaling resulted in a switch from a contractile to a synthetic state in vascular smooth muscle cells.
• Silencing of miR-21 using lentivirus effectively prevented the formation of TAAD induced by AngII in the mouse model.
• Therapeutic approaches for TAAD need to account for potential side effects related to changes in TGF-β signaling.

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