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Workshop: endothelial cell dysfunction leading to diabetic nephropathy : focus on nitric oxide
M S Goligorsky1, J Chen, S Brodsky
1Departments of Medicine, Physiology, and Biophysics, and the Program on Biomedical Engineering, State University of New York, Stony Brook, USA. mgoligorsky@mail.som.sunysb.edu
Hypertension (Dallas, Tex. : 1979)
|March 7, 2001
Summary
Diabetic nephropathy stems from microangiopathy. Endothelial cell dysfunction, initiated by glucose scavenging nitric oxide, is a common pathway for diabetic complications, offering new prevention strategies.
Area of Science:
- Nephrology
- Endocrinology
- Cardiovascular Research
Background:
- Diabetic nephropathy is a manifestation of diabetic microangiopathy.
- The Steno hypothesis provides a foundation for understanding diabetic complications.
Purpose of the Study:
- To propose endothelial cell dysfunction as a common pathophysiological pathway in diabetic complications.
- To elucidate the mechanisms initiating and maintaining endothelial dysfunction in diabetes.
Main Methods:
- Review of existing literature and hypotheses.
- Pathophysiological analysis of molecular mechanisms involved in endothelial dysfunction.
Main Results:
- Glucose scavenging of nitric oxide is proposed as the initiation phase of endothelial dysfunction.
- Advanced glycated end products and plasminogen activator inhibitor-1 contribute to the maintenance phase.
- Decreased endothelial nitric oxide synthase expression and reduced nitric oxide generation are critical in maintaining endothelial dysfunction.
Conclusions:
- Endothelial cell dysfunction is a unifying pathophysiological pathway for diabetic complications.
- Understanding this pathway may lead to novel prevention strategies for diabetic complications.