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Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
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Urea-induced ROS cause endothelial dysfunction in chronic renal failure.
Maria D'Apolito1, Xueliang Du2, Daniela Pisanelli3
1Institute of Pediatrics, University of Foggia, Foggia Viale Pinto 1, O.O.R.R., Foggia, Italy.
Atherosclerosis
|February 16, 2015
Summary
Urea in chronic renal failure (CRF) directly harms arterial cells, increasing oxidative stress and inflammation. This study shows urea causes endothelial dysfunction, contributing to atherosclerosis in CRF patients.
Area of Science:
- Cardiovascular Biology
- Renal Medicine
- Oxidative Stress Research
Background:
- Accelerated atherosclerosis is common in chronic renal failure (CRF), but its mechanisms are unclear.
- Urea, elevated in CRF, is hypothesized to increase reactive oxygen species (ROS) production in endothelial cells.
Purpose of the Study:
- To investigate if CRF-associated urea levels increase ROS production in human aortic endothelial cells (HAEC).
- To determine if urea-induced ROS contribute to endothelial dysfunction and proatherogenic pathways.
Main Methods:
- HAEC were exposed to 20mM urea.
- Mice underwent 5/6 nephrectomy (uremia model) and were treated with a ROS scavenger (MnTBAP).
Main Results:
- Urea induced mitochondrial ROS production in HAEC, inhibiting GAPDH and activating inflammatory pathways.
- Urea-induced ROS reduced PGI2 synthase activity and caused ER stress.
- MnTBAP treatment in uremic mice prevented oxidative stress and pro-inflammatory marker expression.
Conclusions:
- Urea at CRF levels directly causes endothelial dysfunction.
- Urea activates proatherogenic pathways via ROS production, contributing to atherosclerosis in CRF.
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