Perivascular Adipose Tissue as an Indication, Contributor to, and Therapeutic Target for Atherosclerosis

Abstract

Perivascular adipose tissue (PVAT) has been identified to have significant endocrine and paracrine functions, such as releasing bioactive adipokines, cytokines, and chemokines, rather than a non-physiological structural tissue. Considering the contiguity with the vascular wall, PVAT could play a crucial role in the pathogenic microenvironment of atherosclerosis. Growing clinical evidence has shown an association between PVAT and atherosclerosis. Moreover, based on computed tomography, the fat attenuation index of PVAT was verified as an indication of vulnerable atherosclerotic plaques. Under pathological conditions, such as obesity and diabetes, PVAT shows a proatherogenic phenotype by increasing the release of factors that induce endothelial dysfunction and inflammatory cell infiltration, thus contributing to atherosclerosis. Growing animal and human studies have investigated the mechanism of the above process, which has yet to be fully elucidated. Furthermore, traditional treatments for atherosclerosis have been proven to act on PVAT, and we found several studies focused on novel drugs that target PVAT for the prevention of atherosclerosis. Emerging as an indication, contributor to, and therapeutic target for atherosclerosis, PVAT warrants further investigation.

Perivascular Adipose-Derived Exosomes Reduce Foam Cell Formation by Regulating Expression of Cholesterol Transporters

“…Based on these studies, it can be concluded that under physiological conditions, PVAT possesses anti-inflammatory characteristics and inhibits the development of atherosclerosis. By contrast, under pathological conditions, such as obesity and diabetes, PVAT becomes dysfunctional and secrets pro-inflammatory adipokines that induce endothelial dysfunction and inflammatory cell infiltration, thus contributing to atherosclerosis ( 9 , 10 ). In this study, we focus on the association between healthy PVAT and macrophage foam cell formation.…”

Role of ferroptosis-related genes in coronary atherosclerosis and identification of key genes: integration of bioinformatics analysis and experimental validation

“…Atherosclerosis is caused by the accumulation of lipidrich macrophages in the subendothelial region of the vascular system. Macrophage accumulation in the subendothelial area of the arterial wall, and the lipid-rich cells promote an inflammatory response and leads to a variety of fatal pathological consequences [40][41][42]. Ferroptosis has been connected to a range of cardiovascular diseases, including heart failure, ischemia-reperfusion injury, and adriamycin cardiotoxicity [43][44][45][46].…”

Association between carotid artery perivascular fat density and cerebral small vessel disease

“…Although the relationship between carotid artery disease and CSVD has been gradually revealed [ 13 – 15 ], the pathophysiologic mechanisms underlying the relationship between pericarotid fat and CSVD have not been fully established. Increasing studies have identified that perivascular fat has endocrine and paracrine functions, and the pathophysiological characteristics seem to be distinct in different anatomical locations and metabolic statuses [ 7 , 8 , 16 ].…”