Background: Epicardial adipose tissue (EAT), a source of adipokines, is metabolically active.
The role of EAT mitochondria in coronary artery disease (CAD) has not been established.
Here we investigated the association between mitochondrial function in EAT and coronary
atherosclerosis. Methods and Results: We obtained EAT samples from CAD patients (n = 14) and non-CAD patients (n = 11)
who underwent coronary artery bypass surgeries or other cardiac surgeries. The mitochondrial
oxidative phosphorylation (OXPHOS) capacities with non-fatty acid and fatty acid substrates
in the EAT measured by the high-resolution respirometry were significantly reduced
in the CAD patients compared to the non-CAD patients. In contrast, there was no significant
difference in mitochondrial reactive oxygen species emission in the EAT between the
groups, that was measured by the spectrofluorometry. The lowered mitochondrial OXPHOS
capacities in the EAT closely correlated with the severity of coronary artery stenosis
evaluated by Gensini score. Intriguingly, the adiponectin release from the EAT was
significantly reduced in the CAD patients, and this correlated with the lowered mitochondrial
OXPHOS capacities in the EAT. Conclusions: The mitochondrial respiratory capacity in EAT was impaired in the CAD patients in
association with the severity of coronary artery stenosis. Our data support the hypothesis
that mitochondrial dysfunction in EAT contributes to the progression of coronary atherosclerosis,
at least in part via reduced adiponectin secretion in EAT.
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