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Titolo:
Abnormal cardiac and skeletal muscle mitochondrial function in pacing-induced cardiac failure
Autore:
Marin-Garcia, J; Goldenthal, MJ; Moe, GW;
Indirizzi:
Mol Cardiol & Neuromuscular Inst, Highland Pk, NJ 08904 USA Mol Cardiol & Neuromuscular Inst Highland Pk NJ USA 08904 k, NJ 08904 USA Univ Toronto, St Michaels Hosp, Terrance Donnelly Heart Cre, Toronto, ON M5B 1W8, Canada Univ Toronto Toronto ON Canada M5B 1W8 t Cre, Toronto, ON M5B 1W8, Canada
Titolo Testata:
CARDIOVASCULAR RESEARCH
fascicolo: 1, volume: 52, anno: 2001,
pagine: 103 - 110
SICI:
0008-6363(200110)52:1<103:ACASMM>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; IDIOPATHIC DILATED CARDIOMYOPATHY; INDUCED HEART-FAILURE; CYTOCHROME-C-OXIDASE; FACTOR-ALPHA; MULTIPLE DELETIONS; RESPIRATORY-CHAIN; DNA DELETIONS; DOGS; MYOCYTES;
Keywords:
energy metabolism; heart failure; mitochondria;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Marin-Garcia, J Mol Cardiol & Neuromuscular Inst, 75 Raritan Ave, HighlandPk, NJ 08904 USA Mol Cardiol & Neuromuscular Inst 75 Raritan Ave Highland Pk NJ USA 08904
Citazione:
J. Marin-Garcia et al., "Abnormal cardiac and skeletal muscle mitochondrial function in pacing-induced cardiac failure", CARDIO RES, 52(1), 2001, pp. 103-110

Abstract

Background: Previous studies have shown that marked changes in myocardial mitochondrial structure and function occur in human cardiac failure. To further understand the cellular events and to clarify their role in the pathology of cardiac failure, we have examined mitochondrial enzymatic function and peptide content, and mitochondrial DNA (mtDNA) integrity in a canine model of pacing-induced cardiac failure. Methods: Myocardium and skeletal muscle tissues were evaluated for levels of respiratory complex I-V and citratesynthase activities, large-scale mtDNA deletions as well as peptide content of specific mitochondrial enzyme subunits. Levels of circulating and cardiac tumor necrosis factor-alpha (TNF-alpha), and of total aldehyde content in left ventricle were also assessed. Results: Specific activity levels of complex III and V were significantly lower in both myocardial and skeletal muscle tissues of paced animals compared to controls. In contrast, activitylevels of complex I, II, IV and citrate synthase were unchanged, as was the peptide content of specific mitochondrial enzyme subunits. Large-scale mtDNA deletions were found to be more likely present in myocardial tissue of paced as compared to control animals, albeit at a relatively low proportionof mtDNA molecules (<0.01% of wild-type). In addition, the reduction in complex III and V activities was correlated with elevated plasma and cardiac TNF-alpha levels. Significant increases in left ventricle aldehyde levels were also found. Conclusions: Our data show reductions in specific mitochondrial respiratory enzyme activities in pacing-induced heart failure which isnot likely due to overall decreases in mitochondrial number, or necrosis. Our findings suggest a role for mitochondrial dysfunction in the pathogenesis of cardiac failure and may indicate a commonality in the signaling for pacing-induced mitochondrial dysfunction in myocardial and skeletal muscle. Increased levels of TNF-alpha and oxidative stress appear to play a contributory role. (C) 2001 Elsevier Science B.V. All rights reserved.

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Documento generato il 14/07/20 alle ore 18:07:27