NDT Advance Access originally published online on June 25, 2007
Nephrology Dialysis Transplantation 2007 22(10):2775-2777; doi:10.1093/ndt/gfm380
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
A breakthrough in diabetic nephropathy: the role of endothelial dysfunction*
1The Division of Nephrology, University of Florida, Gainesville FL 32610 and 2Pathology and Laboratory Medicine Service, North Florida/South Georgia Veterans Health System, and Department of Pathology, Immunology and Laboratory Medicine, University of Florida, Gainesville, FL 32608, USA
Correspondence and offprint requests to: Takahiko Nakagawa, MD, PhD, Division of Nephrology, Hypertension and Transplantation, University of Florida, PO Box 100224, Gainesville FL 32610-0224. Email: nakagt@medicine.ufl.edu
Keywords: mesangiolysis; glomerular microaneurysm; KimmelSteil-Wilson nodule; VEGF; eNOS; animal model
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| Summary of key findings |
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Kanetsuna et al. [1] have published an important paper in the American Journal of Pathology, reporting that renal lesions resembling human diabetic nephropathy can be induced in mice made diabetic (with streptozotocin) which genetically lack endothelial nitric oxide synthase (eNOS). eNOS is a key enzyme in endothelial cells that produces nitric oxide (NO). In turn, NO has multiple functions in the vasculature, including acting as a vasodilator, anti-inflammatory, anti-thrombotic and anti-proliferative activities. In this study, diabetic eNOS knockout mice developed both renal functional (proteinuria, reduced glomerular filtration rate) and structural changes consistent with human diabetic nephropathy. Up to now, it has been difficult to develop in mice models of diabetic nephropathy that
| Review of the field |
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| What is in it for the practicing nephrologist? |
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| Take home message |
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