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Cellular Senescence and the Associated Secretome Contribute to Age‐Related Vascular Dysfunction

Age‐related vascular dysfunction (e.g., large elastic artery [aorta] stiffening and endothelial dysfunction) is mediated by excess reactive oxygen species (ROS) leading to lower nitric oxide (NO) bioavailability. The upstream mechanisms mediating excess ROS are mostly unknown. Cellular senescence is a principal mechanism of aging and the senescence associated secretory phenotype (SASP) may exacerbate ROS.