|Exercise-induced adaptations of cardiac redox homeostasis and remodeling in heterozygous SOD2-knockout mice.|
|PMID: 21836049 Owner: NLM Status: MEDLINE|
|A reduced expression of the manganese-dependent superoxide dismutase (SOD2) is characterized by increased cardiac oxidative stress. Oxidative stress has also been described in situations of physical exercise. We investigated the influence of physical exercise (EX; treadmill 1 h/day at 15 m/min, 5 days/wk, at an angle of 5° for a duration of 8 wk) on cardiac function [heart frequency (HF), echocardiography, morphometry], oxidative stress [reactive oxygen species (ROS)], and antioxidative defence capacity (peroxiredoxin 1-6) in male SOD2-knockout (SOD2_EX) and wild-type mice (WT_EX) compared with untrained age-matched animals (WT_CON; SOD2_CON). In SOD2_CON, heart weight, cardiomyocyte diameter, and cardiac ROS were significantly larger and peroxiredoxin isoforms 4-6 lower than in WT_CON. The vessel-to-cardiomyocyte ratio, cardiac VEGF-concentration, and cardiac function were similar in SOD2_CON and WT_CON. Both groups tolerated the exercise protocol well. In WT, exercise significantly increased vessel-to-cardiomyocyte ratio and ROS-generation and downregulated peroxiredoxin isoforms 4-6 and VEGF generation. The vessel-to-cardiomyocyte ratio, cardiac VEGF concentration, and cardiac ROS were not altered in SOD2_EX compared with SOD2_CON, but a significant upregulation of cardiac peroxiredoxin 1 and 4 was observed. Similar to the result observed in WT_EX, peroxiredoxin 3 was upregulated in SOD2_EX. Chronic exercise shifted the (mal)adaptive hypertrophic into a compensated dilated cardiac phenotype in SOD2_EX. In conclusion, downregulation of SOD2 induces a maladaptive cardiac hypertrophy. In this situation, physical exercise results in a further deterioration of cardiac remodeling despite an upregulation of the antioxidative defense system.|
|L Richters; N Lange; R Renner; N Treiber; A Ghanem; K Tiemann; K Scharffetter-Kochanek; W Bloch; K Brixius|
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|Type: Journal Article Date: 2011-08-11|
|Title: Journal of applied physiology (Bethesda, Md. : 1985) Volume: 111 ISSN: 1522-1601 ISO Abbreviation: J. Appl. Physiol. Publication Date: 2011 Nov|
|Created Date: 2011-11-18 Completed Date: 2012-06-05 Revised Date: 2013-09-26|
Medline Journal Info:
|Nlm Unique ID: 8502536 Medline TA: J Appl Physiol (1985) Country: United States|
|Languages: eng Pagination: 1431-40 Citation Subset: IM|
|Dept. of Molecular and Cellular Sport Medicine, German Sport Univ. Cologne, Carl-Diem-Weg 6, 50933 Cologne, Germany.|
|APA/MLA Format Download EndNote Download BibTex|
Antioxidants / metabolism
Apoptosis / genetics
Cardiomegaly / genetics, metabolism, physiopathology
Heart / physiology*
Myocytes, Cardiac / metabolism, physiology
Oxidative Stress / genetics, physiology
Peroxiredoxins / genetics
Physical Conditioning, Animal / physiology*
Reactive Oxygen Species / metabolism
Superoxide Dismutase / deficiency, genetics*
Vascular Endothelial Growth Factor A / metabolism
Ventricular Remodeling / genetics, physiology*
|0/Antioxidants; 0/Protein Isoforms; 0/Reactive Oxygen Species; 0/Vascular Endothelial Growth Factor A; 0/vascular endothelial growth factor A, mouse; EC 184.108.40.206/Peroxiredoxins; EC 220.127.116.11/Superoxide Dismutase; EC 18.104.22.168/superoxide dismutase 2|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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