Interestingly, this protein has been observed to exacerbate MVP phenotype, being involved in its pathogenesis via various direct and indirect mechanisms, namely: induction of reactive oxygen species; endothelial cells migration with increased valvular endothelial cells endothelial-to-mesenchymal transition (also overexpressing BMP-4); collagen production; MMP-9 overexpression; valvular interstitial cells proliferation; and proteoglycans overexpression (38). Here, MMP9 is linked to familial mitral valve prolapse.