This study aims to demonstrate the role of stress-induced senescence in aged-related neointimal formation. We demonstrated that aging increases senescence associated galactosidase activity (SA--Gal) after vascular injury and the subsequent neointimal formation (Neointima to Media ratio : 0.8 ± 0.2 vs. 0.54 ± 0.15) in rats. We found that senescent cells (SA--Gal⁺ p21⁺) were scattered throughout the media and adventitia of the vascular wall at day 7 after injury and reached their maximum number at day 14. However, senescent cells only persisted in the injured arteries of aged animals until day 30. No senescent cells were observed in the non-injured, contralateral artery. Interestingly, vascular senescent cells accumulated genomic 8-oxo-G, indicating that these cells were under intense oxidative stress. To demonstrate whether senescence worsens intimal hyperplasia after injury, we seeded matrigel-embedded senescent and non-senescent vascular smooth muscle cells (VSMC) around injured vessels. The neointima was thicker in arteries treated with senescent cells with respect to those that received normal cells (Neointima to Media ratio: 0.41 ± 0.105 vs. 0.26 ± 0.04). In conclusion, these results demonstrate that vascular senescence is not only a consequence of post-injury oxidative stress but is also a worsening factor for neointimal development in the aging vasculature.