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

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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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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