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(Circulation. 2004;110:242-243.)
© 2004 American Heart Association, Inc.

Editorial

Gene Therapy in Congestive Heart Failure

Casilde Sesti, PhD; Robert A. Kloner, MD, PhD

From The Heart Institute, Good Samaritan Hospital, University of Southern California, Los Angeles.

Correspondence to Robert A. Kloner, The Heart Institute, Good Samaritan Hospital, University of Southern California, 1225 Wilshire Blvd, Los Angeles, CA 90017-2395. E-mail Rkloner@goodsam.org

Key Words: Editorials • genes • heart failure

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

Although research and development of gene therapy have encountered several difficulties in recent years, they have also begun to show potential for the treatment of acquired and inherited human diseases. Gene therapy may have wide applicability for the treatment of numerous cardiovascular diseases, including congestive heart failure (CHF), ischemic heart disease, and cardiomyopathy. CHF remains a leading cause of death and morbidity in industrialized nations, and the number of patients with CHF continues to increase as the population ages. Pharmacological therapies control symptoms, reduce left ventricular (LV) dilation, improve function, and reduce mortality. These therapies control the disease but do not cure it. Currently, however, the growing knowledge of molecular mechanisms involved in myocardial dysfunction has allowed the identification of potential therapeutic targets designed with the aim of curing CHF. Several studies in animal models have provided hope that gene therapy may be one of the future strategies for the treatment of clinical CHF. In these studies, myocardial gene transfer has been used to target at least 3 different biological pathways that play a crucial role in the pathophysiology of CHF: Intracellular calcium signaling, ß₁-adrenergic receptor (ß₁-AR) signaling, and antiapoptotic signaling. The activity of sarcoplasmic reticulum Ca²⁺ ATPase (SERCA2a) is decreased in failing myocardium, and this results in abnormal Ca²⁺ handling.¹ In an animal model of heart failure, Miyamoto et al² showed that in vivo overexpression of SERCA2a, achieved by catheter injection of an adenovirus carrying the SERCA2a gene into the aortic root, restored systolic and diastolic function . . . [Full Text of this Article]

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