Abstract

Excessive matrix metalloproteinase (MMP) activity during inflammation disrupts aortic wall homeostasis, causing progression of thoracic aortic aneurysms and dissections (TAAD). The NLRP3-ASC-caspase-1 inflammasome complex is critically involved in the activation and secretion of inflammatory factors. However, the role of this complex in regulating MMP activity remains unknown. We hypothesize that the NLRP3 inflammasome complex activates MMP-9, leading to cleavage of contractile proteins, resulting in thoracic aortic smooth muscle cell (SMC) dysfunction.

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