Decreased peroxisome proliferator-activated receptor gamma expression levels in pericoronary adipose tissue adjacent to atherosclerotic plaque compared to lesion-free coronary arteries

Pericoronary adipose tissue (PCAT) regulates arterial homeostasis, is considered to act in paracrine manner, and plays a role in the pathogenesis of atherosclerosis. The nuclear receptor Peroxisome Proliferator-Activated receptor gamma (PPARγ) is a key regulator of adipogenesis, and alterations of its function are associated with different pathological processes related to metabolic syndrome and inflammatory response.

To investigate whether the PCAT surrounding coronary occlusive atherosclerotic lesions shows specific PPARγ expression pattern compared to PCAT surrounding plaque-free segments

We enrolled 47 patients (32 men, aged 68±12 years old) with 3-vessel coronary artery disease (CAD) who underwent elective coronary bypass surgery. A control group of 10 age- and sex-matched patients with severe valvular disease who underwent aortic or mitral valve replacement was also included (8 men, aged 67±15 years old). PCAT samples were received from all participants. In patients with CAD, the PCAT was harvested from two sites: adjacent to an occlusive atherosclerotic coronary lesion, and a plaque-free segment. PPARγ expression levels in PCAT cells were quantified by real-time reverse transcription polymerase chain reaction.

PCAT analysis showed a significant downregulation of PPARγ expression levels in CAD compared to non-CAD patients (45±19 versus 93±15, p=0.01). In addition, PPARγ levels showed significantly lower expression in PCAT from around atherosclerotic plaque compared to lesion-free sites (31±12 versus 45±19, p=0.04). Notably, the expression of PPARγ from atherosclerotic plaque showed robust negative correlations with BMI (r=−0.47, p=0.001).

PPARγ in PCAT surrounding coronary occlusive atherosclerotic lesions are significantly downregulated and their levels are associated with patients' BMI. Our study opens new perspectives in the pathophysiologic role of PCAT in atherosclerotic complications of diabetes and should be further investigated.

Type of funding sources: None.