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Overactivated bradykinin–B2 receptor promotes type a aortic dissection by inducing endothelial dysfunction: Therapeutic effect of icatibant
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DOI：10.1016/j.lfs.2026.124572.png)
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Abstract
En 中文
Type A aortic dissection (TAAD) is a life-threatening cardiovascular emergency for which no effective pharmacological therapy currently exists. Elevated bradykinin (BK) has been identified as an independent predictor of poor postoperative outcomes in TAAD patients. However, whether and how elevated BK contributes to TAAD pathogenesis remains unknown. Here, we aimed to delineate the mechanistic role of BK and its receptors in TAAD pathogenesis.
Keywords:
Type A aortic dissection
Bradykinin
Icatibant
Oxidative stress
Endothelial dysfunction
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