Modulation of pro-inflammatory status of visceral fat: A novel therapeutic perspective for cardiovascular disease

Obesity’s prevalence worldwide has steadily increased over the past decades, reaching epidemiological proportions in Western Countries. Obesity has been recognised as an independent risk factor for metabolic disorders including insulin resistance, type 2 diabetes, dyslipidemia as well as for cardiovascular diseases (CVD). Adipose tissue (AT) is a dynamic organ which expansion in obesity leads to aberrant lipid release and cytokines production, that ultimately determine a low-grade chronic inflammatory state. Moreover, aging influences AT homeostasis with a significant age-related increase in fat mass, redistribution of body fat with increase in visceral AT and decline in subcutaneous AT, as well as ectopic fat deposition. All these age-related AT changes contribute to worse health conditions in the elderly. Several experimental and epidemiological studies showed that the link between obesity, especially visceral obesity, and CVD might be represented by the systemic pro-inflammatory status triggered by obesity .Different approaches had been designed to target obesity-related inflammation and, consecutively, to lower the CVD associated risk. In this review we highlight the present strategies that might control CVD risk by lowering visceral AT depots, throughout regulating AT inflammation.