Editorials |
From Cardiac Surgery (R.F.K.) and Cardiology (E.O.M.), Veterans Affairs Medical Center, University of Minnesota, Minneapolis; and the Mitochondrial Research Unit (W.S.), Erasmus Medical Center, Rotterdam, The Netherlands.
Correspondence to Edward O. McFalls, MD, PhD, Cardiology (111C), Veterans Affairs Medical Center, 1 Veterans Dr, Minneapolis, MN 55417. E-mail mcfal001@umn.edu
See related article, pages 103–112
Key Words: myocardial hibernation mitochondria preconditioning superoxide heart failure
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
| Introduction |
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In the current issue, Page et al12 demonstrate that the process of hibernation is associated with altered expression of mitochondrial proteins. Using 2D differential-in-gel electrophoresis and matrix-assisted laser desorption ionization time-of-flight mass spectrometry in a swine model of hibernation, they have found that key mitochondrial proteins associated with the electron transport chain are reduced. The functional importance of the decreased protein expression is documented by reduced activity measurements of the pyruvate dehydrogenase complex, cytochrome c oxidase, and citrate synthase. The parallel reductions in mitochondrial proteins and contractile function 5 months after placement of the coronary artery constrictor suggest that the "downregulation" of electron transport
Related Article:
Circ. Res. 2008 102: 103-112.
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