Mitochondrial Oxidative Phosphorylation defect in the Heart of Subjects with Coronary Artery Disease.

ABSTRACT: Coronary artery disease (CAD) is a leading cause of death worldwide and frequently associated with mitochondrial dysfunction. Detailed understanding of abnormalities in mitochondrial function that occur in patients with CAD is lacking. We evaluated mitochondrial damage, energy production, and mitochondrial complex activity in human non-CAD and CAD hearts. Fresh and frozen human heart tissue was used. Cell lysate or mitochondria were isolated using standard techniques. Mitochondrial DNA (_mtDNA), NAD + and ATP levels, and mitochondrial oxidative phosphorylation capacity were evaluated. Proteins critical to the regulation of mitochondrial metabolism and function were also evaluated in tissue lysates. PCR analysis revealed an increase in _mtDNA lesions and the frequency of

SUBMITTER: Ait-Aissa K 

PROVIDER: S-EPMC6527853 | biostudies-literature | 2019 May

REPOSITORIES: biostudies-literature