Aging was associated with the medial wall thickening of renal interlobar arteries, that was in a large part prevented in CalpTG mice (Fig. 4A,B,E, p = 0.0015). Similarly, aorta medial wall surface was less increased with aging in CalpTG mice, in contrast with WT mice (Fig. 4C,D,F, p = 0.0011). CalpTG mice were also protected against the heart remodelling that occurs with aging (Fig. 4G, p = 0.015). The modifications in heart weight were actually due to cardiomyocyte hypertrophy since morphometric analyses evidenced that the number of cardiomyocyte nuclei/surface decreased with aging, but to a lower extent in CalpTG mice (Fig. 4H, p = 0.0002).Figure 4Calpastatin overexpression protects against cardiovascular aging. Mean media surface of interlobar arteries was significantly less increased in CalpTG (TG) mice at 2 years in comparison to WT mice (A,B,E, **p < 0.01, n = 10/group, magnification ×400). Similarly, aorta remodelling was less important in CalpTG mice (C,D,F, **p < 0.01, n = 10/group, magnification ×200). Heart weight increased with aging but less in CalpTG mice than in WT animals (G, *p < 0.05, n = 10/group). This increase in heart weight was due to cellular hypertrophy since the number of nuclei per field at 400x magnification was significantly lower in WT in comparison to CalpTG mice (H, ***p < 0.001, n = 5/group).