(Circulation. 2000;101:1498.)
© 2000 American Heart Association, Inc.
Editorial |
From the Institute of Molecular Cardiobiology, Johns Hopkins University School of Medicine, Baltimore, Md.
Correspondence to Eduardo Marbán, MD, PhD, Institute of Molecular Cardiobiology, Johns Hopkins University School of Medicine, Room 844, Ross Bldg, 720 Rutland Ave, Baltimore, MD 21205. E-mail marban@jhmi.edu
Key Words: Editorials gene therapy heart diseases
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Then the queenly Circe spoke in words and addressed me: You will come first of all to the Sirens, who are enchanters of all mankind and whoever comes their way; and that man who unsuspecting approaches them, and listens to the Sirens singing, has no prospect of coming home. You must drive straight on past... Homer, The Odyssey
The prospect of using genes as therapeutic agents presents myriad opportunities. No physician could fail to appreciate the power of this approach: why not abandon the shackles of the limited pharmacological and device repertoire and focus instead on reengineering the culprit tissue by somatic gene transfer? The explosion of genomic information leaves us with an embarrassment of riches in terms of potential therapeutic agents. Why draw the line at natures own genes expressed in their usual settings? Genes can readily be tailored to exhibit special properties not found in nature, altering the function of their protein products for specific ends. Alternatively, wild-type genes can be expressed in tissues where they are normally silent.
In this issue, Weig et al1 describe a clever
application of the latter approach: V2 vasopressin receptor genes,
usually expressed only in kidney, were delivered to
myocardium packaged in recombinant adenoviruses. Expression
of these adenyl cyclaseactivating receptors in the
myocardium converted the basal negative inotropic response
to infused vasopressin into a positive one. Because vasopressin levels
are elevated in heart failure, a situation in which ß-receptors are
uncoupled from cyclase,2 ectopic expression of V2
receptors would logically be predicted
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