Age-related increases in chronic, low-grade inflammation and reactive oxygen species (ROS)-mediated oxidative stress drive the hallmarks of aging including mitochondrial dysfunction, dysregulated energy sensing and cellular senescence and changes in circulating factors, another fundamental aging mechanism. Together, these upstream processes contribute to arterial dysfunction (i.e., endothelial dysfunction and large elastic artery stiffening) by reducing the bioavailability of the vasodilatory molecule nitric oxide (NO) which ultimately leads to the development of cardiovascular diseases (CVD).