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(Hypertension. 2004;43:720.)
© 2004 American Heart Association, Inc.

Editorial Commentaries

Smart Gene Therapy for the Heart

From the Department of Physiology and Biophysics, Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson.

Correspondence to Dr David E. Stec, Assistant Professor, Department of Physiology and Biophysics, Center for Excellence in Cardiovascular-Renal Research, 2500 North State Street, Jackson, MS 39216-4505. E-mail dstec@physiology.umsmed.edu

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

The ultimate goal in the treatment of myocardial infarction (MI) is the delivery of therapeutic agents in a timely fashion that would be able to protect the heart from the deleterious effects of prolonged ischemia or the effects of repeated bouts of ischemia. The ideal agent would "know" when to become active, specifically in the affected area of the heart to limit side effects, and could be turned "off" after the ischemia is resolved. This "smart" approach would allow for treatment to protect the specific region of the heart most at risk for damage during ischemia while at the same time ending the therapy when the ischemic incident is resolved. This type of approach would foster rapid treatment with minimal outside intervention during the critical early phase of MI.

In this issue of Hypertension, Tang et al describe a novel gene therapy system for ischemic heart injury using an ischemia-sensing biosensor to activate the expression of a therapeutic gene (heme oxygenase-1 [HO-1]), which acts to limit the extent of ischemic injury.¹ Because expression of the HO-1 gene is under the control of the ischemia biosensor, its expression is then subsequently turned off after the tissue is adequately oxygenated when proper blood flow is restored to the heart. This permits gene expression to be controlled at an unprecedented level, driven specifically by the pathological stimulus and lasting only as long as the stimulus persists.

The ischemic biosensor developed by Tang et al is composed of an oxygen-sensing transactivator (OST), which . . . [Full Text of this Article]