Figure 4.

Arterial aneurysm can be induced by excessive production of the proteases by SMCs, phenotype switching of SMCs, and loss of SMCs, which lead to the arterial media destruction, the arterial wall thinning, an increase in wall stress and artery segment dilatation. Both hyalinization and lipid deposition in atherosclerotic CAAs result in the disturbance of the inner and medial layers in vessel wall, the muscular elastic components destruction, the vascular wall weakening and elasticity decreasing, allowing the reduction of vessel's tolerance, as well as vascular dilatation and aneurysm. In KD-associated CAAs, inflammation, genetic factors and MMPs activity lead to breakdown of elastin, degradation of the connective tissue proteins and vessel wall matrix, weakening vascular wall, finally inducing CAAs.