Why the study?
The underlying causes of myocardial metabolic alterations, and the functional consequences of cardiac mitochondrial protein acetylation on metabolic changes and myocardial dysfunction, remain poorly understood.
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Design
Review
Should not yet change metabolic therapy in heart disease; leaves open site-specific functional links between acetylation and cardiac energetics.
Perturbations in myocardial energy substrate metabolism are key contributors to the pathogenesis of heart diseases. However, the underlying causes of these metabolic alterations remain poorly understood. Recently, post-translational acetylation-mediated modification of metabolic enzymes has emerged as one of the important regulatory mechanisms for these metabolic changes. Nevertheless, despite the growing reports of a large number of acetylated cardiac mitochondrial proteins involved in energy metabolism, the functional consequences of these acetylation changes and how they correlate to metabolic alterations and myocardial dysfunction are not clearly defined. This review summarizes the evidence for a role of cardiac mitochondrial protein acetylation in altering the function of major metabolic enzymes and myocardial energy metabolism in various cardiovascular disease conditions.
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Ketema et al. (2021) studied this question.
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