Affiliation:
1. Department of Molecular Physiology and Biophysics
2. Vanderbilt Institute for Integrative Biosystems Research and Education, 6301 Stevenson Center, Vanderbilt University, VU Station B 351807
3. Department of Biomedical Engineering
4. Department of Physics and Astronomy, Vanderbilt University, Nashville TN 37235, USA
Abstract
The heart is well known as a metabolic omnivore in that it is capable of consuming fatty acids, glucose, ketone bodies, pyruvate, lactate, amino acids and even its own constituent proteins, in order of decreasing preference. The energy from these substrates supports not only mechanical contraction, but also the various transmembrane pumps and transporters required for ionic homeostasis, electrical activity, metabolism and catabolism. Cardiac ischemia - for example, due to compromise of the coronary vasculature or end-stage heart failure - will alter both electrical and metabolic activity. While the effects of myocardial ischemia on electrical propagation and stability have been studied in depth, the effects of ischemia on metabolic substrate preference has not been fully appreciated: oxygen deprivation during ischemia will significantly alter the relative ability of the heart to utilize each of these substrates. Although changes in cardiac metabolism are understood to be an underlying component in almost all cardiac myopathies, the potential contribution of amino acids in maintaining cardiac electrical conductance and stability during ischemia is underappreciated. Despite clear evidence that amino acids exert cardioprotective effects in ischemia and other cardiac disorders, their role in the metabolism of the ischemic heart has yet to be fully elucidated. This review synthesizes the current literature of the metabolic contribution of amino acids during ischemia by analyzing relevant historical and recent research.
Subject
General Biochemistry, Genetics and Molecular Biology
Cited by
99 articles.
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