Nakajima 2017 Europ Heart J

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Mitochondrial dysfunction in epicardial adipose tissue; possible role in progression of coronary artery disease.

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Nakajima T, Yokota T, Shingu Y, Yamada A, Iba Y, Ujihara K, Takada S, Shirakawa R, Furihata T, Tsuda M, Matsumoto J, Fukushima A, Matsui Y, Kinugawa S (2017)

Event: Europ Heart J

Epicardial adipose tissue (EAT) is an ectopic fat surrounding the heart within the pericardium, most of which locates around the coronary artery. Recently, EAT has shown to be accumulated in coronary artery disease (CAD). However, the role of its functional changes in CAD remains unknown. Here, we tested the hypothesis that impaired mitochondrial oxidative phosphorylation (OXPHOS) capacity in the EAT might contribute to progression of CAD.

We obtained EAT samples during open-heart surgery from CAD patients (n=14) who underwent coronary artery bypass grafting and non-CAD patients (n=11) who underwent other cardiac surgeries unrelated to atherosclerotic disease. We measured mitochondrial OXPHOS capacity in the permeabilized EAT by using a high-resolution respirometry. Mitochondrial complex I-linked OXPHOS capacity in the EAT was significantly decreased in CAD patients compared to non-CAD patients by 31%. In addition, CAD patients had lowered capacities of complex I-linked OXPHOS and complex I+II-linked OXPHOS under the existence of fatty acids in the EAT compared to non-CAD patients by 35%, respectively. In addition, the impaired mitochondrial OXPHOS capacities in the EAT were closely correlated with severity of CAD evaluated by the Gensini score. We also measured EAT volume by computed tomography before the surgery, which was larger in CAD patients than non-CAD patients (70.5±31.1 cm3 vs. 29.8±24.1 cm3, P<0.01). However, there was no significant correlation between EAT volume and severity of CAD. Intriguingly, protein content of adiponectin, which has protective action in the progression of atherosclerosis, was significantly decreased in the EAT from CAD patients, and the decreased adiponectin content was correlated with the impaired mitochondrial OXPHOS capacities in the EAT.

Mitochondrial OXPHOS capacities in the EAT was impaired in CAD patients. The impaired mitochondrial OXPHOS capacities in the EAT, but not EAT volume, were associated with severity of CAD. Our data support the hypothesis that mitochondrial dysfunction in the EAT plays a crucial role in the progression of CAD in association with reduced adiponectin secretion from the EAT.


Bioblast editor: Kandolf G O2k-Network Lab: JP Sapporo Yokota T


Labels: MiParea: Respiration  Pathology: Cardiovascular 

Organism: Human  Tissue;cell: Fat  Preparation: Permeabilized tissue 


Coupling state: OXPHOS  Pathway: F, N, NS  HRR: Oxygraph-2k