Vitamin D puts the brakes on angiotensin II-induced oxidative stress and vascular smooth muscle cell senescence.

Signaling via both vitamin D (VitD) and the renin-angiotensin system (RAS) plays important roles in physiological processes. Evidence has mounted linking cardiovascular disease to both increased activity of the RAS and VitD deficiency. Although several studies have established functional relationships between the RAS and VitD, many aspects of their complex interaction remain unknown. In this issue of Atherosclerosis, Valcheva and colleagues show that defective VitD signaling can promote vascular damage by inducing premature senescence of smooth muscle cells due to elevated local production of angiotensin II and reactive oxygen species, and upregulation of the tumor suppressor p57(Kip2).