Gene silencing or inhibition of Sp1/Sp3 led to severe endothelial dysfunction and hypertension, and overexpression of Sp1/Sp3 ameliorated endothelial senescence and apoptosis induced by Ang II; this suggests that Sp1/Sp3 may represent potential targets for drug design to treat cardiovascular diseases. The gene discussed is SP1; the disease is endothelial dysfunction.