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本文引用的文献

1
Long-term in vivo resistin overexpression induces myocardial dysfunction and remodeling in rats.长期体内抵抗素过表达可诱导大鼠心肌功能障碍和重构。
J Mol Cell Cardiol. 2011 Aug;51(2):144-55. doi: 10.1016/j.yjmcc.2011.04.006. Epub 2011 Apr 23.
2
Pitavastatin prevents postprandial endothelial dysfunction via reduction of the serum triglyceride level in obese male subjects.匹伐他汀通过降低肥胖男性受试者的血清甘油三酯水平来预防餐后内皮功能障碍。
Heart Vessels. 2011 Jul;26(4):428-34. doi: 10.1007/s00380-010-0071-7. Epub 2010 Dec 4.
3
Cross-talk between adipose tissue and vasculature: role of adiponectin.脂肪组织与血管之间的串扰:脂联素的作用。
Acta Physiol (Oxf). 2011 Sep;203(1):167-80. doi: 10.1111/j.1748-1716.2010.02216.x. Epub 2010 Dec 8.
4
Regulatory action on rosiglitazone by the U.S. Food and Drug Administration.美国食品药品监督管理局对罗格列酮采取的监管行动。
N Engl J Med. 2010 Oct 14;363(16):1489-91. doi: 10.1056/NEJMp1010788. Epub 2010 Sep 23.
5
Modest visceral fat gain causes endothelial dysfunction in healthy humans.适量内脏脂肪增加可导致健康人群的内皮功能障碍。
J Am Coll Cardiol. 2010 Aug 17;56(8):662-6. doi: 10.1016/j.jacc.2010.03.063.
6
Epicardial perivascular adipose-derived leptin exacerbates coronary endothelial dysfunction in metabolic syndrome via a protein kinase C-beta pathway.心外膜血管周脂肪组织来源的瘦素通过蛋白激酶 C-β通路加重代谢综合征患者的冠状动脉内皮功能障碍。
Arterioscler Thromb Vasc Biol. 2010 Sep;30(9):1711-7. doi: 10.1161/ATVBAHA.110.210070. Epub 2010 Jun 24.
7
Resistin decreases expression of endothelial nitric oxide synthase through oxidative stress in human coronary artery endothelial cells.抵抗素通过氧化应激降低人冠状动脉内皮细胞内皮型一氧化氮合酶的表达。
Am J Physiol Heart Circ Physiol. 2010 Jul;299(1):H193-201. doi: 10.1152/ajpheart.00431.2009. Epub 2010 Apr 30.
8
Interleukin-6 inhibits endothelial nitric oxide synthase activation and increases endothelial nitric oxide synthase binding to stabilized caveolin-1 in human vascular endothelial cells.白细胞介素-6 抑制内皮型一氧化氮合酶的激活,并增加人血管内皮细胞中内皮型一氧化氮合酶与稳定化 caveolin-1 的结合。
J Hypertens. 2010 May;28(5):940-51. doi: 10.1097/HJH.0b013e32833992ef.
9
Caveolin-1 limits the contribution of BK(Ca) channel to EDHF-mediated arteriolar dilation: implications in diet-induced obesity.窖蛋白-1 限制 BK(Ca)通道对 EDHF 介导的小动脉舒张的贡献:在饮食诱导肥胖中的意义。
Cardiovasc Res. 2010 Sep 1;87(4):732-9. doi: 10.1093/cvr/cvq088. Epub 2010 Mar 17.
10
Adipose tissue angiogenesis as a therapeutic target for obesity and metabolic diseases.脂肪组织血管生成作为肥胖和代谢性疾病的治疗靶点。
Nat Rev Drug Discov. 2010 Feb;9(2):107-15. doi: 10.1038/nrd3055.

肥胖症中的微血管反应性:治疗干预的意义。

Microvascular responsiveness in obesity: implications for therapeutic intervention.

机构信息

Department of Pharmacology, University of Oxford, UK Department of Physiology, New York Medical College, Valhalla, New York, USA.

出版信息

Br J Pharmacol. 2012 Feb;165(3):544-60. doi: 10.1111/j.1476-5381.2011.01606.x.

DOI:10.1111/j.1476-5381.2011.01606.x
PMID:21797844
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3315030/
Abstract

UNLABELLED

Obesity has detrimental effects on the microcirculation. Functional changes in microvascular responsiveness may increase the risk of developing cardiovascular complications in obese patients. Emerging evidence indicates that selective therapeutic targeting of the microvessels may prevent life-threatening obesity-related vascular complications, such as ischaemic heart disease, heart failure and hypertension. It is also plausible that alterations in adipose tissue microcirculation contribute to the development of obesity. Therefore, targeting adipose tissue arterioles could represent a novel approach to reducing obesity. This review aims to examine recent studies that have been focused on vasomotor dysfunction of resistance arteries in obese humans and animal models of obesity. Particularly, findings in coronary resistance arteries are contrasted to those obtained in other vascular beds. We provide examples of therapeutic attempts, such as use of statins, ACE inhibitors and insulin sensitizers to prevent obesity-related microvascular complications. We further identify some of the important challenges and opportunities going forward.

LINKED ARTICLES

This article is part of a themed section on Fat and Vascular Responsiveness. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2012.165.issue-3.

摘要

未加标签

肥胖对微循环有不利影响。微血管反应性的功能变化可能会增加肥胖患者发生心血管并发症的风险。新出现的证据表明,选择性地针对微血管进行治疗可能预防危及生命的肥胖相关血管并发症,如缺血性心脏病、心力衰竭和高血压。脂肪组织微循环的改变也可能导致肥胖的发生。因此,靶向脂肪组织小动脉可能是减少肥胖的一种新方法。本综述旨在研究最近关注肥胖人群和肥胖动物模型阻力动脉血管舒缩功能障碍的研究。特别地,我们将冠状动脉阻力动脉的研究结果与其他血管床的研究结果进行对比。我们提供了一些治疗尝试的例子,如使用他汀类药物、ACE 抑制剂和胰岛素增敏剂来预防肥胖相关的微血管并发症。我们进一步确定了一些重要的挑战和机遇。

相关文章

本文是脂肪和血管反应性专题的一部分。要查看该部分中的其他文章,请访问 http://dx.doi.org/10.1111/bph.2012.165.issue-3。