Proinflammatory phenotype of perivascular adipocytes

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Perivascular adipose tissue (PVAT) directly abuts the lamina adventitia of conduit arteries and actively communicates with the vessel wall to regulate vascular function and inflammation. Mounting evidence suggests that the biological activities of PVAT are governed by perivascular adipocytes, a unique class of adipocyte with distinct molecular and phenotypic characteristics. Perivascular adipocytes surrounding human coronary arteries (pericoronary perivascular adipocytes) exhibit a reduced state of adipogenic differentiation and a heightened proinflammatory state, secreting ≤50-fold higher levels of the proinflammatory cytokine monocyte chemoattractant peptide-1 compared with adipocytes from other regional depots. Thus, perivascular adipocytes may contribute to upregulated inflammation of PVAT observed in atherosclerotic human blood vessels. However, perivascular adipocytes also secrete anti-inflammatory molecules such as adiponectin, and elimination of PVAT in rodent models has been shown to augment vascular disease, suggesting that some amount of PVAT is required to maintain vascular homeostasis. Evidence in animal models and humans suggests that inflammation of PVAT may be modulated by environmental factors, such as high-fat diet and tobacco smoke, which are relevant to atherosclerosis. These findings suggest that the inflammatory phenotype of PVAT is diverse depending on sp

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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