Vitamin D May Shield Blood Vessels From Damage Linked to Heart Disease
Researchers have identified a potential mechanism by which vitamin D protects the delicate inner lining of blood vessels from a destructive enzyme called heparanase. Since endothelial damage drives cardiovascular disease — the world's leading cause of death — this finding could reshape how companies develop heart drugs and influence public health vitamin D recommendations.
Originaltitel: Heparanase, Endothelial Dysfunction, and Cardiovascular Risk: The Emerging Role of Vitamin D.
Heparanase, ett enzym som bryter ned endotelglykokalyx, framträder som en central målpunkt för att förebygga kärlväggsdysfunktion och hjärt-kärlsjukdom. Överskottsaktivet av heparanase försvagar kärlskyddet och bidrar till hjärtinfarkt, hjärtsvikt och ateroskleros. En svensk-indisk forskargrupp vid Örebro University och GITAM University visar att vitamin D kan bevara glykokalyxstrukturen och bromsa heparanaseuttrycket, vilket tidigare påvisats i njurceller. Genom att dämpa glykokaylxnedbrytning kan vitamin D potentiellt minska endoteldysfunktion och kardiovaskulär risk. Fynden öppnar möjlighet till nutritionsbaserad interventionsstruktur för kardiovaskulär prävention. För inköpschefer och kliniker innebär detta utredning av vitamin D-statusen hos högriskpatienter samt potentiella supplementprotokolls implementering i läkemedelsplaneringen.
Endothelial dysfunction is a central pathophysiological mechanism in the development of cardiovascular disease (CVD), the leading global cause of morbidity and mortality. Vascular homeostasis critically depends on the endothelial glycocalyx, which regulates vascular permeability, mechanotransduction, and anti-inflammatory signaling. Heparanase, the only known mammalian endoglycosidase capable of cleaving heparan sulfate, plays a pivotal role in glycocalyx degradation, a process exacerbated by oxidative stress, hyperglycemia, and hypertension. Excessive heparanase activity has been implicated in several cardiovascular pathologies, including heart failure, ischemia-reperfusion injury, and atherosclerosis, yet effective therapeutic strategies remain limited. Emerging evidence suggests that vitamin D may preserve endothelial integrity by maintaining the structure of the glycocalyx and suppressing heparanase expression, as demonstrated in podocytes. By attenuating heparanase-mediated degradation of the glycocalyx in the vasculature and heart, vitamin D could exert protective effects against endothelial dysfunction and thereby mitigate cardiovascular risk.