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.

Highlights

  • Atherosclerosis is an inflammatory disease of the arteries characterized by lipid accumulation within the artery walls

  • Dysfunctional white adipose tissue (WAT) might be positively associated with atherosclerosis development, whereas activation of brown adipose tissue (BAT) may protect against atherosclerosis development

  • We further demonstrate that brown adipocyte-specific peroxisome proliferator-activated receptor-γ (PPAR-γ) deletion impairs Perivascular adipose tissue (PVAT) development and enhances atherosclerosis in mice suggesting that PPAR-γ could be a pivotal link between PVAT and atherosclerosis lesion development [184]

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Summary

Introduction

Atherosclerosis is an inflammatory disease of the arteries characterized by lipid accumulation within the artery walls. Secretion of adiponectin is reduced, whereas secretion of pro-inflammatory cytokines is increased, leading to enhanced local inflammation and substantially affecting cardiovascular function and morphology.

Results
Conclusion

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