title: Beta blocker specificity: a building block toward personalized medicine.
abstract: Drugs known as beta blockers, which antagonize the beta-adrenergic receptor (beta-AR), are an important component of the treatment regimen for chronic heart failure (HF). However, a significant body of evidence indicates that genetic heterogeneity at the level of the beta(1)-AR may be a factor in explaining the variable responses of HF patients to beta blockade. In this issue of the JCI, Rochais et al. describe how a single amino acid change in beta(1)-AR alters its structural conformation and improves its functional response to carvedilol, a beta blocker currently used in the treatment of HF (see the related article beginning on page 229). This may explain why some HF patients have better responses not only to carvedilol but to certain other beta blockers as well. The data greatly enhance our mechanistic understanding of myocardial adrenergic signaling and support the development of "tailored" or "personalized" medicine, in which specific therapies could be prescribed based on a patient's genotype.
authors.affiliation: Center for Translational Medicine and George Zallie and Family Laboratory for Cardiovascular Gene Therapy, Department of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
authors.forename: Brent R
authors.initials: BR
authors.lastname: DeGeorge
authors.forename: Walter J
authors.initials: WJ
authors.lastname: Koch
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D015195:Drug Design; D006333:Heart Failure / Q000188:drug therapy*; D006801:Humans; D018342:Receptors, Adrenergic, beta-1 / Q000187:drug effects / Q000235:genetics; D015398:Signal Transduction
chemical_list: D000319:Adrenergic beta-Antagonists; D018342:Receptors, Adrenergic, beta-1