title: Pathological and physiological hypertrophies are regulated by distinct gene programs.
abstract: BACKGROUND
  This study aims to investigate changes that occur during progression and establishment of physiological and pathological cardiac hypertrophy, by microarray technology and functional annotations.
  
  
  METHODS
  Myocardial infarction leading to heart failure was induced in rats, with animals killed 1, 3, 7, 14, 42, and 92 days after coronary artery ligation. A second group was subjected to daily treadmill exercise and killed 1, 4, 24, and 48 h after a single exercise bout, or after 28 or 56 days of exercise training.
  
  
  RESULTS
  Physiological hypertrophy was associated with less transcriptional alternation than pathological hypertrophy, indicating that posttranscriptional and translational regulation may be more important. The main difference between the two types of hypertrophy was that myocardial infarction was associated with downregulation of genes related to fatty acid metabolism, whereas no such change occurred after exercise training. Thus, fatty acid metabolism may distinguish adverse maladaptive hypertrophy from beneficial adaptive hypertrophy.
  
  
  CONCLUSIONS
  This study points to specific genes and gene classes related to biological processes that may be important in these well-characterized rat models of physiological and pathological cardiac hypertrophy.
authors.affiliation: Department of Circulation and Medical Imaging, Norwegian University of Science and Technology, Trondheim, Norway. vidar.beisvag@ntnu.no
authors.forename: Vidar
authors.initials: V
authors.lastname: Beisvag
authors.forename: Ole Johan
authors.initials: OJ
authors.lastname: Kemi
authors.forename: Ingerid
authors.initials: I
authors.lastname: Arbo
authors.forename: Jan Pål
authors.initials: JP
authors.lastname: Loennechen
authors.forename: Ulrik
authors.initials: U
authors.lastname: Wisløff
authors.forename: Mette
authors.initials: M
authors.lastname: Langaas
authors.forename: Arne Kristian
authors.initials: AK
authors.lastname: Sandvik
authors.forename: Øyvind
authors.initials: Ø
authors.lastname: Ellingsen
mesh_terms: D000222:Adaptation, Physiological / Q000235:genetics; D000818:Animals; D006332:Cardiomegaly / Q000235:genetics* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D016000:Cluster Analysis; D004195:Disease Models, Animal; D005227:Fatty Acids / Q000378:metabolism; D005260:Female; D020869:Gene Expression Profiling / Q000379:methods; D005786:Gene Expression Regulation; D006333:Heart Failure / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D050356:Lipid Metabolism / Q000235:genetics; D009203:Myocardial Infarction / Q000150:complications / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D020411:Oligonucleotide Array Sequence Analysis; D005082:Physical Exertion; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013997:Time Factors; D014158:Transcription, Genetic
chemical_list: D005227:Fatty Acids