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Gene therapy for a broken heart

03.01.04 | JCI Journals

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The presence of S16EPLN upregulated the activity of the enzyme SERCA2 in transduced cells and compensated for defects in calcium uptake during heart failure. Echocardiographic and hemodynamic measurements showed improvements in global heart function and contractility in rats that received S16EPLN treatment. In addition, the formation of scar tissue was suppressed in these animals. Although further long-term studies are necessary to clarify the effects of modifying phospholamban on arrhythmias, gene transfer of S16EPLN shows promise as a novel therapeutic strategy.

TITLE: Chronic phospholamban inhibition prevents progressive cardiac dysfunction and pathological remodeling after infarction in rats

AUTHOR CONTACT:
John Ross Jr.
University of California, San Diego, La Jolla, California, USA.
Phone: 858-822-2267
Fax: 858-534-1626
E-mail: jross@ucsd.edu

View the PDF of this article at: http://www.jci.org/cgi/content/full/113/5/727

Journal of Clinical Investigation

Keywords

Article Information

Contact Information

Brooke Grindlinger
science_editor@the-jci.org

How to Cite This Article

APA:
JCI Journals. (2004, March 1). Gene therapy for a broken heart. Brightsurf News. https://www.brightsurf.com/news/86GOQ66L/gene-therapy-for-a-broken-heart.html
MLA:
"Gene therapy for a broken heart." Brightsurf News, Mar. 1 2004, https://www.brightsurf.com/news/86GOQ66L/gene-therapy-for-a-broken-heart.html.