Epicardial adipose tissue (EAT), the fat depot that directly surrounds the heart and is contained beneath the pericardium, has recently acquired increasing scientific interest. The discovery of its endocrine role, exerted through cytokines and adipokines secretion, opened the way to the investigation of its potential paracrine crosstalk with the underlying myocardium. Indeed, EAT features have been extensively correlated to onset and progression of cardiovascular pathologies, such as coronary heart disease (CHD). EAT also represents a source of adipose stem cells (ASCs), characterized by multipotent differentiation capacity. Remarkably, epicardial ASCs (e-ASCs) have been reported to have a higher cardiomyogenic potential as compared to pericardial and omental ASCs subtypes, and to exert paracrine proangiogenic and immunomodulatory effects. However, little is known about e-ASCs contribution to the milieu affecting cardiac function or to the endogenous repair process in CHD. Notably, studies aimed to investigate the molecular regulation of e-ASCs differentiative and paracrine effects are still lacking. The present project aims to extend current knowledge on e-ASC gene expression profiles by performing an extensive characterization of their differentiation potential and paracrine effects. We also intend to analyze the modulation of selected genes involved in these cellular mechanisms in the context of CHD pathogenesis, with the aim of identifying novel molecules for targeted experimental validation. Our approach will deepen our knowledge about e-ASC functional characteristics and paracrine role in the context of myocardial dysfunction, contributing to ameliorate the clinical treatment of cardiovascular pathologies, through both the identification of novel markers for CHD stratification and prognosis and the design of improved protocols for e-ASC-based cell therapies in CHD patients.
