Could angiotensin‐II induced T‐cell senescence exacerbate age‐related vascular dysfunction?

Abstract

The peer review history is available in the Supporting Information section of this article (https://doi.org/10.1113/ JP282581#support-information-section).Advancing age is a primary, non-modifiable risk factor for the development of cardiovascular diseases (CVDs), which are the leading cause of morbidity and mortality worldwide. CVDs are largely driven by age-related vascular dysfunction which is characterized by two key manifestations: large elastic artery (e.g. aorta) stiffening and vascular endothelial dysfunction. These processes are largely caused by excess reactive oxygen species (ROS)-induced oxidative stress and inflammation which are mutually reinforcing and can reduce the bioavailability of the vasodilatory molecule nitric oxide (NO) (Trott et al. 2021). However, there have been an insufficient number of studies examining the cell type(s) that may induce this age-related increase in inflammation and in turn influence oxidative stress. In a recent publication in The Journal of Physiology, Trott et al. (2021) aimed to determine the role of T-cells in mediating age-related changes in vascular inflammation and associated aortic stiffening and vascular endothelial dysfunction.