Mechanisms of perivascular adipose tissue dysfunction in obesity.
Mechanisms of perivascular adipose tissue dysfunction in obesity.
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DOI：
10.1155/2013/402053
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发表时间：
2013
影响因子：
2.8
通讯作者：
Somoza B
中科院分区：
文献类型：
--
作者：
Fernández-Alfonso MS;Gil-Ortega M;García-Prieto CF;Aranguez I;Ruiz-Gayo M;Somoza B
大多数血管被脂肪组织包围。与外膜相似，血管周围脂肪组织（PVAT）仅被视为血管系统的被动结构支撑，并且在离体血管研究中常规去除。在1991年，Soltis和Cynthia首次证明PVAT减少了大鼠主动脉对去甲肾上腺素的收缩。从那时起，一个重要的数量的脂肪细胞衍生因子的生理和病理生理旁分泌血管活性的影响已被确定。PVAT在肥胖中经历结构和功能变化。在早期饮食诱导的肥胖，适应性过度生产的血管扩张因子发生在PVAT，可能旨在保护血管功能。然而，在确定的肥胖症中，PVAT通过增加收缩、氧化和炎症因子而失去其抗收缩特性，导致内皮功能障碍和血管疾病。本文就PVAT功能障碍在肥胖中的作用机制作一综述。
Most blood vessels are surrounded by adipose tissue. Similarly to the adventitia, perivascular adipose tissue (PVAT) was considered only as a passive structural support for the vasculature, and it was routinely removed for isolated blood vessel studies. In 1991, Soltis and Cassis demonstrated for the first time that PVAT reduced contractions to noradrenaline in rat aorta. Since then, an important number of adipocyte-derived factors with physiological and pathophysiological paracrine vasoactive effects have been identified. PVAT undergoes structural and functional changes in obesity. During early diet-induced obesity, an adaptative overproduction of vasodilator factors occurs in PVAT, probably aimed at protecting vascular function. However, in established obesity, PVAT loses its anticontractile properties by an increase of contractile, oxidative, and inflammatory factors, leading to endothelial dysfunction and vascular disease. The aim of this review is to focus on PVAT dysfunction mechanisms in obesity.