Interestingly, one study has shown that increased H3K4me1 is correlated with LSD1 knockdown, while SUV39H1 is considered to play a weak role in regulating H3K9me2 and H3K4me3 at the Nox4 and eNOS promoters [110], suggesting that LSD1 is a key factor in endothelial dysfunction and that targeting LSD1 may be an important method of reducing diabetes-associated endothelial dysfunction. Here, KDM1A is linked to endothelial dysfunction.