Research Paper Volume 10, Issue 7 pp 1722—1744

Heme oxygenase-1 ameliorates oxidative stress-induced endothelial senescence via regulating endothelial nitric oxide synthase activation and coupling

Figure 8. HO-1 ameliorates H2O2-induced premature senescence in HUVECs via eNOS. HO-1 attenuates H2O2-induced expressions of p53/p21 and ameliorated oxidative stress-induced DNA damage in endothelia senescence through two mechanisms: 1) HO-1 prevents eNOS uncoupling by inhibiting ROS. 2) Interaction between HO-1 and eNOS makes eNOS easier to interact with Akt, for which Akt can phosphorylate eNOS at Ser1177.