This is based on the following observations: (1) overexpression of ΔHO-1, a truncated HO-1 without TMS which was found to accumulate in the nucleus, inhibited H2O2-induced endothelial senescence (Fig. 2); (2) overexpression of nuclear HO-1 by infection of Ad-ΔHO-1(3NLS) could still preserve the inhibitory effect against endothelial senescence even though endogenous HO-1 was knocked down by CRISPR/Cas9 (Fig. 3); and (3) repression of HO-1 nuclear translocation by silencing of SPP exacerbated endothelial senescence (Fig. 4). Here, HMOX1 is linked to infection.