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Carbamylated low-density lipoprotein induces endothelial dysfunction.

Thimoteus Speer1, Frederick O Owala2, Erik W Holy2

  • 1University Heart Center, Cardiovascular Center, University Hospital Zurich, Rämistrasse 100, 8091 Zurich, Switzerland Center of Molecular Cardiology, Schlieren Campus, University of Zurich, Zurich, Switzerland Department of Internal Medicine 4, Saarland University Hospital, Homburg/Saar, Germany.

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|March 25, 2014
PubMed
Summary
This summary is machine-generated.

Carbamylation of low-density lipoproteins (LDL) impairs endothelial function and increases cardiovascular risk in chronic kidney disease (CKD) patients. This study reveals a novel mechanism in atherosclerosis pathogenesis.

Keywords:
CarbamylationEndothelial functionLipoproteinNitric oxideReactive oxygen species

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Area of Science:

  • Cardiovascular Research
  • Atherosclerosis Pathogenesis
  • Endothelial Dysfunction

Background:

  • Cardiovascular events are a leading cause of death, with atherosclerosis driven by low-density lipoproteins (LDL).
  • Carbamylation of LDL, particularly in chronic kidney disease (CKD), may alter lipoprotein function.
  • The impact of carbamylated LDL on endothelial function is not well understood.

Purpose of the Study:

  • To investigate the effect of carbamylated LDL (cLDL) on endothelial function.
  • To elucidate the mechanisms underlying cLDL-induced endothelial dysfunction.
  • To assess the prognostic value of LDL carbamylation in CKD patients.

Main Methods:

  • Isolated and carbamylated native LDL (nLDL).
  • Assessed vascular reactivity in mouse aortic rings and measured reactive oxygen species (ROS) and nitric oxide (NO) production.
  • Correlated LDL carbamylation levels with cardiovascular outcomes in CKD patients.

Main Results:

  • Carbamylated LDL impaired endothelium-dependent relaxation and increased ROS production.
  • cLDL activated NADPH-oxidase and promoted eNOS uncoupling via S-glutathionylation.
  • LOX-1 receptor exacerbated cLDL-induced endothelial dysfunction.
  • Higher LDL carbamylation levels predicted cardiovascular events and mortality in CKD patients.

Conclusions:

  • LDL carbamylation induces endothelial dysfunction through LOX-1 activation and ROS generation, leading to eNOS uncoupling.
  • This represents a novel mechanism in atherosclerosis development.
  • LDL carbamylation is pathogenic and prognostic in CKD patients with elevated cLDL levels.