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(Circulation Research. 2007;101:227.)
© 2007 American Heart Association, Inc.

Editorials

Endothelial NF-B As a Mediator of Kidney Damage

The Missing Link Between Systemic Vascular and Renal Disease?

Tomasz J. Guzik, David G. Harrison

From the Emory University Division of Cardiology, Department of Medicine, Atlanta, Ga; and the Atlanta Veterans Administration Hospital, Ga.

Correspondence to David G. Harrison, Division of Cardiology, Emory University, 101 Woodruff Circle, WMBR 319, Atlanta, GA 30322. E-mail dharr02@emory.edu

See related article, page 268–276

Key Words: molecular biology • monocytes • monocyte chemoattractant protein-1 • nitric oxide • NF-B • oxidative stress

An extract of the first 250 words of the full text is provided, because this article has no abstract.

In the current issue of Circulation Research Henke and coworkers demonstrate a critical role for the transcription factor nuclear factor-kappaB (NF-B) in the genesis of renal damage caused by hypertension.¹ The authors created mice in which the NF-B superrepressor IBN was induced in the endothelium using Cre/Lox technology. They then exposed these mice and appropriate controls to a rather complex model of hypertension involving angiotensin II infusion, high salt and inhibition of endogenous nitric oxide production. Although the NF-B superrepressor did not prevent hypertension, it markedly diminished renal injury. Albuminuria in the NF-B suppressed mice was reduced by half, perivascular and tubular fibrosis was decreased, TNF- levels were diminished and the renal infiltration of inflammatory cells reduced. The study illustrates a previously unappreciated role of the endothelium and specifically endothelial NF-B in coordinating numerous aspects of hypertensive renal damage.

Prevention of hypertension and its attendant end organ damage is one of the major therapeutic aims in cardiovascular medicine. A vast amount of research has been devoted to understanding the mechanisms and pathogenesis of hypertension, but for the past two decades this knowledge has not led to new treatments. Although current drugs are effective in many patients, there are still numerous patients in whom even combination therapies are not successful.² Moreover while we focus almost solely on bringing the blood pressure levels back to normal, the mechanisms of end-organ damage are in part independent of blood pressure and are influenced by factors such as . . . [Full Text of this Article]