title: Regular exercise or changing diet does not influence aortic valve disease progression in LDLR deficient mice.
abstract: BACKGROUND
  The development and progression of calcific aortic valve disease (CAVD) shares a number of similarities with atherosclerosis. Recently we could demonstrate that regular exercise training (ET) as primary prevention prevents aortic valve disease in LDL-receptor deficient (LDLR(-/-)) mice. We aimed to investigate the impact of exercise training on the progression of CAVD in LDLR(-/-) mice in the setting of secondary prevention
  
  
  RESULTS
  Sixty-four LDLR(-/-) mice were fed with high cholesterol diet to induce aortic valve sclerosis. Thereafter the animals were divided into 3 groups: group 1 continuing on high cholesterol diet, group 2 continuing with cholesterol diet plus 1 h ET per day, group 3 continuing with normal mouse chow. After another 16 weeks the animal were sacrificed. Histological analysis of the aortic valve thickness demonstrated no significant difference between the three groups (control 98.3±4.5 µm, ET 88.2±6.6 µm, change in diet 87.5±4.0). Immunohistochemical staining for endothelial cells revealed a disrupted endothelial cell layer to the same extend in all groups. Furthermore no difference between the groups was evident with respect to the expression of inflammatory, fibroblastic and osteoblastic markers.
  
  
  CONCLUSIONS
  Based on the present study we have to conclude that once the development of a CAVD is initiated, exercise training or a change in diet does not have the potential to attenuate the progress of the CAVD.
authors.affiliation: University of Leipzig-Heart Center Leipzig, Department of Internal Medicine/Cardiology, Leipzig, Germany.
authors.forename: Florian
authors.initials: F
authors.lastname: Schlotter
authors.forename: Yasuharu
authors.initials: Y
authors.lastname: Matsumoto
authors.forename: Norman
authors.initials: N
authors.lastname: Mangner
authors.forename: Gerhard
authors.initials: G
authors.lastname: Schuler
authors.forename: Axel
authors.initials: A
authors.lastname: Linke
authors.forename: Volker
authors.initials: V
authors.lastname: Adams
mesh_terms: D000818:Animals; D001021:Aortic Valve / Q000473:pathology / Q000503:physiopathology; D001024:Aortic Valve Stenosis / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D015415:Biomarkers / Q000378:metabolism; D001783:Blood Flow Velocity; D001835:Body Weight; D002114:Calcinosis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control; D004032:Diet; D018450:Disease Progression; D004730:Endothelium, Vascular / Q000473:pathology; D050356:Lipid Metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D018384:Oxidative Stress; D005082:Physical Exertion; D044140:Receptor, Angiotensin, Type 1 / Q000378:metabolism; D011973:Receptors, LDL / Q000172:deficiency* / Q000235:genetics; D055502:Secondary Prevention
chemical_list: D015415:Biomarkers; D044140:Receptor, Angiotensin, Type 1; D011973:Receptors, LDL