title: Skeletal muscle protein metabolism in human heart failure.
abstract: OBJECTIVE
  This review considers evidence that the clinical condition of heart failure alters skeletal muscle protein synthesis and/or breakdown to promote skeletal muscle wasting and functional decrements that ultimately contribute to the symptomology of the disease.
  
  
  RESULTS
  Advanced HF is frequently accompanied by muscle atrophy and a cachectic phenotype. Protein metabolic derangements that promote this phenotype are understudied and poorly understood. Instead, most investigations have evaluated regulatory hormones/signaling pathways thought to be reflective of protein synthesis and breakdown. Several of these recent studies have provided exciting data suggesting that the dysfunctional myocardium releases catabolic agents that could promote the skeletal muscle myopathic phenotype either directly or through modulation of other regulatory systems (e.g., energy balance).
  
  
  CONCLUSIONS
  Although our understanding of skeletal muscle atrophy and dysfunction in heart failure is limited, recent studies have provided clues about the nature and timing of protein metabolic dysfunction. More specifically, skeletal muscle protein metabolic derangements likely evolve during periods of disease-related stress (i.e., acute disease exacerbation and hospitalization) and potentially derive in part, from signals promoted in the damaged/dysfunctional myocardium. Despite these compelling studies, there is a surprising lack of data regarding the nature or timing of specific protein metabolic defects in heart failure.
authors.affiliation: Department of Medicine and Molecular Physiology and Biophysics, University of Vermont, College of Medicine, Burlington, Vermont 05405, USA.
authors.forename: Damien M
authors.initials: DM
authors.lastname: Callahan
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Toth
mesh_terms: D000818:Animals; D002100:Cachexia / Q000150:complications / Q000503:physiopathology; D004195:Disease Models, Animal; D006333:Heart Failure / Q000150:complications / Q000503:physiopathology*; D006706:Homeostasis; D006728:Hormones / Q000378:metabolism; D006801:Humans; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism; D009124:Muscle Proteins / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000378:metabolism*; D009133:Muscular Atrophy / Q000150:complications / Q000503:physiopathology; D055435:Myostatin / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D006728:Hormones; D035683:MicroRNAs; D009124:Muscle Proteins; D055435:Myostatin