title: Model-specific selection of molecular targets for heart failure gene therapy.
abstract: Heart failure (HF) is a complex multifaceted problem of abnormal ventricular function and structure. In recent years, new information has been accumulated allowing for a more detailed understanding of the cellular and molecular alterations that are the underpinnings of diverse causes of HF, including myocardial ischemia, pressure-overload, volume-overload or intrinsic cardiomyopathy. Modern pharmacological approaches to treat HF have had a significant impact on the course of the disease, although they do not reverse the underlying pathological state of the heart. Therefore gene-based therapy holds a great potential as a targeted treatment for cardiovascular diseases. Here, we survey the relative therapeutic efficacy of genetic modulation of β-adrenergic receptor signaling, Ca(2+) handling proteins and angiogenesis in the most common extrinsic models of HF.
authors.affiliation: Department of Surgery, Division of Cardiovascular Surgery, The University of Pennsylvania Medical Center, Philadelphia, PA, USA.
authors.forename: Michael G
authors.initials: MG
authors.lastname: Katz
authors.forename: Anthony S
authors.initials: AS
authors.lastname: Fargnoli
authors.forename: Catherine E
authors.initials: CE
authors.lastname: Tomasulo
authors.forename: Louella A
authors.initials: LA
authors.lastname: Pritchette
authors.forename: Charles R
authors.initials: CR
authors.lastname: Bridges
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D015316:Genetic Therapy / Q000379:methods*; D006321:Heart / Q000503:physiopathology*; D006333:Heart Failure / Q000235:genetics* / Q000503:physiopathology / Q000628:therapy*; D006801:Humans; D017202:Myocardial Ischemia / Q000235:genetics / Q000503:physiopathology / Q000628:therapy; D011943:Receptors, Adrenergic, beta / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology
chemical_list: D011943:Receptors, Adrenergic, beta