Journal Article Comment Epublish
PubMed: 40371651 DOI: 10.1172/JCI193128
Endothelial dysfunction in patients with type 2 diabetes: the truth is in the blood.
J Clin Invest 135(10)
Authors: Sarah Costantino, Shafeeq A Mohammed, Francesco Paneni
Affiliations
- Center for Translational and Experimental Cardiology (CTEC), Department of Cardiology, University Hospital Zurich and University of Zurich, Zurich, Switzerland.
- University Heart Center, Cardiology, University Hospital Zurich, Zurich, Switzerland.
Abstract
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.
MeSH
Diabetes Mellitus, Blood, Endothelium, Diabetes Mellitus, Type 2