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Dysfunctional epicardial adipose tissue (EAT) and maladaptive heart remodeling in patients with increased visceral adiposity: the ST2/IL-33 cardio-fat signaling
Vol 32, Issue 4S1, 2018
Abstract
Recent clinical evidences suggested that the expansion of epicardial adipose tissue (EAT) and its transformation into a pro-inflammatory organ in visceral obesity are related to maladaptive heart remodeling and heart failure (HF). However, the sustained molecular mechanisms are poorly understood. The ST2/IL33 system has recently obtained great attention in the field of cardiovascular diseases due to its cardio-protective role in different stress conditions that can promote cardiomyocyte hyperthrophy and deposition of extracellular proteins (fibrosis). Any imbalance in ST2/IL33 signaling may thus lead toward HF. Discussing how dysfunctional EAT may interfere with the protective role of ST2/IL33 pathway and its association with heart remodeling in visceral obesity are the aims of the present review.
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Medical Genetics, University of Torino Medical School, Italy
Department of Biomedical, Surgical and Dental Sciences, University of Milan, Italy