New research by scientists in Scotland has found that a small piece of genetic material could explain why arteries become increasingly stiff (which happens in high blood pressure) and why blood vessels age faster. If found in patient blood samples, this molecule could give doctors an early warning of artery problems, and help people get treatment more quickly.
The researchers pinpointed a piece of genetic material called a micro-RNA – specifically one called miR-214 – which makes white blood cells called T-cells move to the fatty tissue around arteries. Once in this tissue, the T-cells cause inflammation, causing the artery structure to become damaged and increasing their stiffness. This work is the first to link a cascade of damaging events linked to blood pressure to higher levels of miR-214. Dr Laura Denby, Kidney Research UK Senior Research Fellow and a collaborator in this study, had previously discovered that miR-214 caused kidney scarring, or fibrosis, following injury.
Dr Aisling McMahon, Executive Director of Research, Innovation & Policy at Kidney Research UK, said, “Along with diabetes, high blood pressure is a significant cause of chronic kidney disease (CKD) and kidney failure. This research suggests that miR-214 levels might be useful to identify people whose blood vessels are at risk of damage earlier, and could be a good target to develop new treatments. This is important because preventing high blood pressure could ultimately help us reduce CKD and prevent kidney failure developing.”
Professor Tomasz Guzik and Dr Ryszard Nosalski at the University of Glasgow led the research for this paper, T Cell-Derived miRNA-214 Mediates Perivascular Fibrosis in Hypertension, which was published in the journal Circulation Research.
Professor Guzil and Dr Nosalski said: “In this study we used many in vivo, in vitro as well as translational human approaches to identify how small molecule of microRNA that is present in lymphocytes, white blood cells responsible for fighting infections, can direct these cell to blood vessels. This is responsible, at least in part, for the process of accelerated vascular ageing characterised by stiffer vessels. We have shown this not only in disease models but also provided proof of concept in patients with hypertension. These studies provide important insights how hypertension may interact with inflammation.”
