Perivascular adipose tissue (PVAT) in atherosclerosis: a double-edged sword

Abstract

Perivascular adipose tissue (PVAT), the adipose tissue that surrounds most of the vasculature, has emerged as an active component of the blood vessel wall regulating vascular homeostasis and affecting the pathogenesis of atherosclerosis. Although PVAT characteristics resemble both brown and white adipose tissues, recent evidence suggests that PVAT develops from its own distinct precursors implying a closer link between PVAT and vascular system. Under physiological conditions, PVAT has potent anti-atherogenic properties mediated by its ability to secrete various biologically active factors that induce non-shivering thermogenesis and metabolize fatty acids. In contrast, under pathological conditions (mainly obesity), PVAT becomes dysfunctional, loses its thermogenic capacity and secretes pro-inflammatory adipokines that induce endothelial dysfunction and infiltration of inflammatory cells, promoting atherosclerosis development. Since PVAT plays crucial roles in regulating key steps of atherosclerosis development, it may constitute a novel therapeutic target for the prevention and treatment of atherosclerosis. Here, we review the current literature regarding the roles of PVAT in the pathogenesis of atherosclerosis.

Keywords: Adipokine; Atherosclerosis; Inflammation; Perivascular adipose tissue.

Fig. 1

The role of PVAT in the regulation of atherosclerosis. In normal physiological state, PVAT secret protective adipokines and bioactive molecules such as adiponectin and NO maintain vascular homeostasis. Under pathology condition, unbalanced PVAT-derived adipokines, chemokines and cytokines targets many cell types including ECs, macrophage, T cells and SMCs involved in endothelial dysfunction, immune cells infiltration, smooth muscle cell migration and proliferation which are predominantly implicated in the pathological process of atherosclerosis