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(Hypertension. 2004;43:1173.)
© 2004 American Heart Association, Inc.

Editorial Commentaries

Gene Therapy and Heme Oxygenase Coming of Age

Richard J. Roman

From the Department of Physiology, Medical College of Wisconsin, Milwaukee.

Correspondence to Richard J. Roman, Department of Physiology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53005. E-mail rroman@mcw.edu

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

The article by Yang et al¹ in this issue of Hypertension is noteworthy in that it makes significant contributions in 2 areas. First, the authors describe an approach using retroviral constructs to achieve long-term (up to 5 months) expression of a human heme-oxygenase 1 (HO-1) gene in the liver, kidney, and vasculature of rats in vivo. They also demonstrated that they could knockdown endogenous HO-1 activity in rats by administration of a retrovirus containing a rat HO-1 antisense construct. The second major advance in this study is that it provides new information that further highlights the importance of the HO/CO system as a key modulator of vascular tone in vivo. They found that overexpression of the human HO-1 gene in the rat attenuates the pressor response to intravenous administration of angiotensin II and that knockdown of endogenous HO-1 activity potentiates the pressor response to angiotensin II.

Gene Therapy Approaches in Hypertension Research

The completion of the sequencing of the human, rat, and mouse genomes now provides an unprecedented opportunity for the discovery of new genes, pathways, and drug targets for the treatment of hypertension and associated end-organ damage. Unfortunately, an examination of the publicly available genome databases (eg, LocusLink, Online Medelian Inheritance in Man [OMIM], the Human Genome Organization [HUGO], and the Genome Database [GDB]) reveals that only 5000 of the 30 000 predicted human genes have any inferred function. The challenge is now to attach function to the genome and to identify the genes and pathways involved in human disease. Most of the progress to . . . [Full Text of this Article]

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