Discovery of a mechanism for vascular damage in type 2 diabetes
Small vesicles from red blood cells can transfer harmful molecules to blood vessels, contributing to damage and impairing their function in type 2 diabetes. The findings are reported by researchers affiliated with CMM in a new publication in the Journal of Clinical Investigation.
Blood vessel damage is a common complication in type 2 diabetes, and it is associated with cardiovascular diseases such as heart attacks and strokes. The mechanisms behind blood vessel damage in diabetes are not well understood but a new study conducted by CMM Group Leader and Professor at Karolinska Institutet, John Pernow, reveals that extracellular vesicles from red blood cells contribute to this damage.
John Pernow and his research team found that vesicles from red blood cells in type 2 diabetes patients are more readily taken up by blood vessel cells than in healthy individuals. They discovered that these vesicles carry the signaling molecule arginase, which causes the formation of free oxygen radicals, impairing blood vessel dilation and contributing to diabetes-related vascular complications.
The study found that inhibiting vesicle uptake and blocking arginase activity can counteract harmful effects on blood vessels.
Aida Collado Sánchez, the first author of the study sees the potential of the new findings: “Our results provide a new understanding of how red blood cells contribute to vascular damage in type 2 diabetes and point to possible treatment strategies to counteract these complications,” she says in an article on the Karolinska Institutet news site.
Future research will explore blood vessel changes in patients and test new drugs candidates to block vesicle uptake.
The study was a collaboration with Karolinska University Hospital and funded by several Swedish foundations such as the Swedish Heart-Lung Foundation, the Swedish Research Council, and the Knut and Alice Wallenberg Foundation.
Publication
Erythrocyte-derived extracellular vesicles induce endothelial dysfunction through arginase-1 and oxidative stress in type 2 diabetes.
Collado A, Humoud R, Kontidou E, Eldh M, Swaich J, Zhao A, Yang J, Jiao T, Domingo E, Carlestål E, Mahdi A, Tengbom J, Végvári Á, Deng Q, Alvarsson M, Gabrielsson S, Eriksson P, Zhou Z, Pernow J. J Clin Invest 2025 Mar;():