Graphical abstraction. credit: American Journal of Physiology – Cardiac and Circulatory Physiology (2023). DOI: 10.1152/ajpheart.00337.2023
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Graphical abstraction. credit: American Journal of Physiology – Cardiac and Circulatory Physiology (2023). DOI: 10.1152/ajpheart.00337.2023
New research at the Roy Blunt NextGen Precision Health building has discovered a potential treatment for the root cause of cardiovascular disease in people with type 2 diabetes.
More than 30 million Americans live with type 2 diabetes. One of the common features of diabetes is stiffness and decreased flexibility of blood vessels caused by damage to the endothelial cells of the vasculature.
Over time, this can lead to the development and progression of cardiovascular disease, which is the number one killer of people with diabetes. Because endothelial dysfunction is causally linked to cardiovascular disease, there is a considerable need to identify new therapeutic targets to improve endothelial function in patients with type 2 diabetes.
A team of researchers at the University of Missouri found that neuraminidase activity is elevated in the circulation of type 2 diabetic mice and humans. A series of mechanistic experiments using cultured endothelial cells and isolated blood vessels linked increased neuraminidase to endothelial dysfunction.
“Neuraminidase circulating in the blood is increased in patients with type 2 diabetes, and its presence has been shown to promote endothelial dysfunction, so it could be used as a means to address the cardiovascular complications faced by patients with type 2 diabetes. “It’s important to target this,” he said. Luis Martinez-Lemus, DVM, Ph.D., James O. Davis Distinguished Professor of Cardiovascular Research at the University of Missouri School of Medicine.
The research team also found that neuraminidase inhibition using zanamivir, an orally inhaled drug used to treat influenza viruses, improved endothelial function in diabetic mice.
“This study reveals the molecular mechanisms by which neuraminidase promotes endothelial dysfunction, and these mechanisms could potentially be exploited therapeutically,” said Dr. Jaume Padilla, associate professor of nutrition and exercise physiology at MU. . “This research is extremely important because improving vascular function in people with type 2 diabetes can help them live longer and better lives.”
“Neuraminidase inhibition improves endothelial function in diabetic mice” and “Neuraminidase-induced phosphatidylserine externalization activates ADAM17 and impairs insulin signaling in endothelial cells” have recently been published. American Journal of Physiology – Cardiac and Circulatory Physiology.
For more information:
Christopher A. Foote et al., Neuraminidase inhibition improves endothelial function in diabetic mice. American Journal of Physiology – Cardiac and Circulatory Physiology (2023). DOI: 10.1152/ajpheart.00337.2023
Larissa Ferreira-Santos et al, Neuraminidase-induced externalization of phosphatidylserine activates ADAM17 and impairs insulin signaling in endothelial cells, American Journal of Physiology – Cardiac and Circulatory Physiology (2023). DOI: 10.1152/ajpheart.00638.2023
