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Previous Volume 358:1628-1630 April 10, 2008 Number 15 Next

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Medical students are taught that endothelial dysfunction is relevant to the pathophysiology of diabetic microvascular disease, especially the glomerular defects that are characteristic of diabetic nephropathy. The facts, however, belie a paucity of knowledge about the molecular biology of the glomeruli of humans with type 1 or type 2 diabetes. Which genes are activated in the glomerular endothelial cells of patients with long-term diabetes? Which genes are abnormally suppressed? The extent of our ignorance is impressive. Fortunately, a study recently reported by Isermann et al.¹ remedies, at least in small part, this deficit.

As a consequence of their unique position . . . [Full Text of this Article]

Source Information

From the Keenan Research Centre of the Li Ka Shing Knowledge Institute and the Divisions of Endocrinology and Nephrology, St. Michael's Hospital; and the University of Toronto — both in Toronto.

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