Figure 3.

Schematic representation of redox-dependent Sod2 promoter methylation in aging vascular cells. Aging is associated with a rise in oxidative stress, which favours increased MnSOD antioxidant defense, at least partially via a lower methylation of Sod2; a rise in MnSOD leads to a temporary, compensatory NO-dependent relaxing pathway that preserves endothelial function. This cascade is not observed in mice exposed to a protective cardiovascular environment provided by chronic treatment with the antioxidant catechin or long-term exposure to physical exercise.