Despite improvements in management and therapeutic approach in the last decades, heart failure is still associated with high mortality rates. The sustained enhancement in the sympathetic nervous system tone, observed in patients with heart failure, causes alteration in β-adrenergic receptor signaling and function. This latter phenomenon is the result of several heart failure-related molecular abnormalities involving adrenergic receptors, G-protein-coupled receptor kinases, and β-arrestins. This article summarizes novel encouraging preclinical strategies to reactivate β-adrenergic receptor signaling in heart failure, including pharmacologic and gene therapy approaches, and attempts to translate acquired notions into the clinical setting.
- Heart Failure/genetics
- Polymorphism, Genetic
- Receptors, Adrenergic, beta/genetics
- Signal Transduction