Cellular, molecular and physiological characterization of epicardial adipose tissue

Abstract

One of the main causes of death in today's European and American society is ischemic heart disease. There are several risk factors associated with this disease, such as diabetes mellitus, hypercholesterolemia, smoking, hypertension and obesity (metabolic syndrome). Of these, obesity is the risk factor that is most worrisome due to its increase in adult and child population. However, it is necessary to distinguish between visceral and subcutaneous obesity, since it is the former that is associated mainly with metabolic diseases and consequently ischemic heart disease. One of the visceral tissues that most concern the current scientific community is the epicardial adipose tissue (EAT), due to its clear location on the coronary arteries. Thus, several studies have used different imaging techniques, which determined a clear association between the volume of this tissue and ischemic heart disease. This may be due, in part, to differential expression and secretion of adipokines between EAT and subcutaneous adipose tissue (SAT). Thus, our group, since 2005 has focused on the study of these tissues and it has been observed that the EAT contains different levels of adiponectin, pro-inflammatory cytokines, proteins related to oxidative stress and lipid transport proteins compared with SAT in patients undergoing cardiovascular surgery. The difference between both tissues in patients with ischemic heart disease is also due to the cellular components, since the EAT contains more inflammatory cells than the SAT and smaller cellular component anti-inflammatory, as are the polarized macrophages. To understand the pathophysiological role of EAT in coronary diseases, specifically ischemic heart disease, it is very important to characterize the different cellular types of EAT and SAT in patients with and without ischemic heart disease. Next, to explore the interaction of EAT and SAT cells with vascular tissue cells might help to understand the etiopathogenic role of EAT in the onset and development of major coronary diseases. On the other hand, it is crucial to study how to enhance the secretion of proteins with cardioprotective functions that attenuate or reverse the deleterious role of EAT in coronary disease.