Furthermore, sh-NAT10 triggered SM22α and N-cadherin expression but decreased CD31 and VE-cadherin levels in Ang II-treated HUVECs (Fig. 3F, G), indicating that NAT10 knockdown increases Ang II-induced endothelial dysfunction and EndMT in HUVECs. This evidence concerns the gene PECAM1 and endothelial dysfunction.