Gene therapy for heart failure.
Despite our continued advances in the management of coronary artery disease, there have been no significant reductions in the morbidity or mortality related to end-stage heart failure. The syndrome of heart failure represents a common endpoint for several disease processes, however, at the molecular level there are certain biochemical similarities common to all failing myocardium. Targeting these derangements with gene therapy represents a promising option in the treatment of heart failure. In this review, we will discuss the common biochemical changes that occur in the failing heart, novel therapeutic targets, including the beta-adrenergic receptor system and intracellular calcium regulation, and the vectors and transfer methodology responsible for delivering these transgenes to the myocardium.
Thompson
Richard B
RB
Department of Surgery, Duke University Medical Center, Durham, North Carolina, USA.
Rungwerth
Katrin
K
Koch
Walter J
WJ
D000818:Animals; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000235:genetics / Q000502:physiology; D015316:Genetic Therapy / Q000379:methods*; D005822:Genetic Vectors / Q000235:genetics; D006333:Heart Failure / Q000235:genetics / Q000628:therapy*; D006801:Humans; D008954:Models, Biological; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D011943:Receptors, Adrenergic, beta / Q000235:genetics / Q000502:physiology
D015220:Calcium Channels; D011943:Receptors, Adrenergic, beta; D002118:Calcium