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.
To read this article in full you will need to make a payment
Purchase one-time access:Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online access
One-time access price info
- For academic or personal research use, select 'Academic and Personal'
- For corporate R&D use, select 'Corporate R&D Professionals'
Subscribe:Subscribe to Journal of Cardiac Failure
Already a print subscriber? Claim online access
Already an online subscriber? Sign in
Register: Create an account
Institutional Access: Sign in to ScienceDirect