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Endothelial dysfunction in patients with type 2 diabetes: the truth is in the blood

Sarah Costantino1,2, Shafeeq A Mohammed1, Francesco Paneni1,2

  • 1Center for Translational and Experimental Cardiology (CTEC), Department of Cardiology, University Hospital Zurich and University of Zurich, Zurich, Switzerland.

The Journal of Clinical Investigation
|May 15, 2025
PubMed

Insights

Red blood cells (RBCs) from diabetic patients release extracellular vesicles (EVs) that impair blood vessel function. These RBC-derived EVs transfer the enzyme arginase-1, causing oxidative stress and endothelial dysfunction.

Area of Science:

  • Vascular Biology
  • Diabetology
  • Cellular Mechanisms

Background:

  • Endothelial dysfunction is a key factor in diabetic vascular complications.
  • Red blood cells (RBCs) play a significant role in this dysfunction, but the exact mechanisms are not fully understood.

Purpose of the Study:

  • To elucidate the mechanisms by which RBCs contribute to endothelial dysfunction in diabetes.
  • To identify the role of extracellular vesicles (EVs) in mediating the detrimental effects of RBCs on the endothelium.

Main Methods:

  • Investigated extracellular vesicles (EVs) derived from RBCs (RBC-EVs) of patients with diabetes.
  • Assessed the uptake of RBC-EVs by endothelial cells.
  • Evaluated the impact of RBC-EVs on endothelium-dependent relaxation.
  • Analyzed the transfer of arginase-1 (Arg1) from RBC-EVs to endothelial cells.

Main Results:

  • RBC-EVs from diabetic patients were internalized by endothelial cells.
  • EV-mediated transfer of arginase-1 (Arg1) from RBCs to endothelial cells was identified as a key mechanism.
  • This transfer led to impaired endothelium-dependent relaxation and increased vascular oxidative stress.

Conclusions:

  • Extracellular vesicles (EVs) from diabetic red blood cells (RBCs) mediate endothelial dysfunction.
  • The prooxidant enzyme arginase-1 (Arg1) transfer via RBC-EVs contributes to vascular oxidative stress in diabetes.
  • Targeting RBC-EV uptake presents a potential strategy for preventing diabetic vascular complications.

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