Consistent with previous studies [18], in this study, both in vivo and in vitro experiments proved that H19 silencing further promoted up-regulation of α-SMA and SM22α, and down-regulated MMP-2 and MMP-9 expressions, suggesting that H19 may participate in the pathogenesis of AD by regulating the expressions of MMP-2/-9 and the proliferation, migration, and phenotype transformation of HASMCs. This evidence concerns the gene MMP2 and Alzheimer disease.