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血管周围脂肪组织与内皮细胞在血管张力调节中的比较。

Comparisons between perivascular adipose tissue and the endothelium in their modulation of vascular tone.

机构信息

Institute of Cardiovascular Sciences, University of Manchester, UK.

Maternal and Fetal Health Research Centre, Institute of Human Development, University of Manchester, UK.

出版信息

Br J Pharmacol. 2017 Oct;174(20):3388-3397. doi: 10.1111/bph.13648. Epub 2016 Nov 18.

Abstract

UNLABELLED

The endothelium is an established modulator of vascular tone; however, the recent discovery of the anti-contractile nature of perivascular adipose tissue (PVAT) suggests that the fat, which surrounds many blood vessels, can also modulate vascular tone. Both the endothelium and PVAT secrete vasoactive substances, which regulate vascular function. Many of these factors are common to both the endothelium and PVAT; therefore, this review will highlight the potential shared mechanisms in the modulation of vascular tone. Endothelial dysfunction is a hallmark of many vascular diseases, including hypertension and obesity. Moreover, PVAT dysfunction is now being reported in several cardio-metabolic disorders. Thus, this review will also discuss the mechanistic insights into endothelial and PVAT dysfunction in order to evaluate whether PVAT modulation of vascular contractility is similar to that of the endothelium in health and disease.

LINKED ARTICLES

This article is part of a themed section on Molecular Mechanisms Regulating Perivascular Adipose Tissue - Potential Pharmacological Targets? To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.20/issuetoc.

摘要

未加标签

内皮细胞是血管张力的既定调节剂;然而,最近发现血管周围脂肪组织 (PVAT) 具有抗收缩特性,这表明环绕许多血管的脂肪也可以调节血管张力。内皮细胞和 PVAT 都分泌血管活性物质,调节血管功能。这些因子中的许多因子在内皮细胞和 PVAT 中都很常见;因此,本综述将重点介绍调节血管张力的潜在共同机制。内皮功能障碍是许多血管疾病的标志,包括高血压和肥胖症。此外,在几种心脏代谢疾病中现在也报道了 PVAT 功能障碍。因此,本综述还将讨论内皮细胞和 PVAT 功能障碍的机制见解,以评估血管收缩性的 PVAT 调节是否与健康和疾病中的内皮细胞相似。

相关文章

本文是关于调节血管周围脂肪组织的分子机制-潜在的药理学靶点的专题的一部分?要查看本节中的其他文章,请访问 http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.20/issuetoc.

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