Why the study?
Do extracellular vesicles derived from red blood cells of patients with type 2 diabetes impair endothelial function?
Do extracellular vesicles derived from red blood cells of patients with type 2 diabetes impair endothelial function?
Red blood cell-derived extracellular vesicles from patients with type 2 diabetes impair endothelial function by transferring arginase-1, highlighting a novel mechanism and potential therapeutic target for diabetic vascular complications.
Endothelial dysfunction remains a cornerstone of diabetic vascular complications. RBCs emerge as pivotal players in endothelial dysfunction, yet the underlying mechanisms remain elusive. In this issue of the JCI, Collado et al. show that the detrimental action of RBCs on the endothelium is mediated by extracellular vesicles (EVs). EVs derived from RBCs (RBC-EVs) of patients with diabetes were taken up by the endothelium and were able to impair endothelium-dependent relaxation via an EV-mediated transfer of the prooxidant enzyme arginase-1 (Arg1) from RBCs to endothelial cells. These findings reveal events implicated in vascular oxidative stress and set the stage for personalized approaches preventing RBC-EVs' uptake by the endothelium.
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Costantino et al. (2025) studied this question.
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