Key result
Gene therapy represents a promising option for treating heart failure by targeting biochemical derangements such as the beta-adrenergic receptor system and intracellular calcium regulation.
Gene therapy targeting common biochemical changes in the failing myocardium represents a promising future therapeutic option for end-stage heart failure.
Gene therapy for heart failure remains investigational; leaves open the need for randomized trials on safety and durable efficacy.
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.
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Thompson et al. (2004) conducted a review in Heart failure. Gene therapy was evaluated. Gene therapy represents a promising option for treating heart failure by targeting biochemical derangements such as the beta-adrenergic receptor system and intracellular calcium regulation.
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