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本文引用的文献

1
Cardiac peroxisome proliferator-activated receptor gamma is essential in protecting cardiomyocytes from oxidative damage.心脏过氧化物酶体增殖物激活受体γ对于保护心肌细胞免受氧化损伤至关重要。
Cardiovasc Res. 2007 Nov 1;76(2):269-79. doi: 10.1016/j.cardiores.2007.06.027. Epub 2007 Jul 4.
2
Rosiglitazone evaluated for cardiovascular outcomes--an interim analysis.罗格列酮心血管结局评估——一项中期分析。
N Engl J Med. 2007 Jul 5;357(1):28-38. doi: 10.1056/NEJMoa073394. Epub 2007 Jun 5.
3
Effect of rosiglitazone on the risk of myocardial infarction and death from cardiovascular causes.罗格列酮对心肌梗死风险及心血管原因所致死亡的影响。
N Engl J Med. 2007 Jun 14;356(24):2457-71. doi: 10.1056/NEJMoa072761. Epub 2007 May 21.
4
Macrophage-specific PPARgamma controls alternative activation and improves insulin resistance.巨噬细胞特异性过氧化物酶体增殖物激活受体γ控制替代性激活并改善胰岛素抵抗。
Nature. 2007 Jun 28;447(7148):1116-20. doi: 10.1038/nature05894. Epub 2007 May 21.
5
PPAR-gamma agonists induce the expression of VEGF and its receptors in cultured cardiac myofibroblasts.过氧化物酶体增殖物激活受体γ激动剂可诱导培养的心肌成纤维细胞中血管内皮生长因子及其受体的表达。
Cardiovasc Res. 2007 Apr 1;74(1):140-50. doi: 10.1016/j.cardiores.2007.01.010. Epub 2007 Jan 17.
6
Hypotension, lipodystrophy, and insulin resistance in generalized PPARgamma-deficient mice rescued from embryonic lethality.从胚胎致死性中挽救出来的全身性PPARγ缺陷小鼠中的低血压、脂肪营养不良和胰岛素抵抗。
J Clin Invest. 2007 Mar;117(3):812-22. doi: 10.1172/JCI28859. Epub 2007 Feb 15.
7
Effect of pioglitazone on the expression of inflammatory cytokines in attenuating rat cardiomyocyte hypertrophy.吡格列酮对减轻大鼠心肌细胞肥大中炎性细胞因子表达的影响。
Methods Find Exp Clin Pharmacol. 2006 Dec;28(10):691-6. doi: 10.1358/mf.2006.28.10.1037500.
8
Are thiazolidinediones good or bad for the heart?噻唑烷二酮类药物对心脏有益还是有害?
Curr Diab Rep. 2006 Nov;6(5):378-83. doi: 10.1007/s11892-006-0009-8.
9
The ubiquitin-proteasome system and inflammatory activity in diabetic atherosclerotic plaques: effects of rosiglitazone treatment.泛素-蛋白酶体系统与糖尿病动脉粥样硬化斑块中的炎症活性:罗格列酮治疗的效果
Diabetes. 2006 Mar;55(3):622-32. doi: 10.2337/diabetes.55.03.06.db05-0832.
10
Peroxisome proliferator-activated receptor-gamma ligands attenuate brain natriuretic peptide production and affect remodeling in cardiac fibroblasts in reoxygenation after hypoxia.过氧化物酶体增殖物激活受体γ配体可减弱脑钠肽的产生,并影响缺氧后复氧时心脏成纤维细胞的重塑。
Cell Biochem Biophys. 2006;44(1):65-71. doi: 10.1385/CBB:44:1:065.

过氧化物酶体增殖物激活受体-γ 在心血管系统中的作用。

PPAR-gamma in the Cardiovascular System.

机构信息

Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.

出版信息

PPAR Res. 2008;2008:745804. doi: 10.1155/2008/745804.

DOI:10.1155/2008/745804
PMID:18288291
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2225467/
Abstract

Peroxisome proliferator-activated receptor-gamma (PPAR-gamma), an essential transcriptional mediator of adipogenesis, lipid metabolism, insulin sensitivity, and glucose homeostasis, is increasingly recognized as a key player in inflammatory cells and in cardiovascular diseases (CVD) such as hypertension, cardiac hypertrophy, congestive heart failure, and atherosclerosis. PPAR-gamma agonists, the thiazolidinediones (TZDs), increase insulin sensitivity, lower blood glucose, decrease circulating free fatty acids and triglycerides, lower blood pressure, reduce inflammatory markers, and reduce atherosclerosis in insulin-resistant patients and animal models. Human genetic studies on PPAR-gamma have revealed that functional changes in this nuclear receptor are associated with CVD. Recent controversial clinical studies raise the question of deleterious action of PPAR-gamma agonists on the cardiovascular system. These complex interactions of metabolic responsive factors and cardiovascular disease promise to be important areas of focus for the future.

摘要

过氧化物酶体增殖物激活受体-γ(PPAR-γ)是脂肪生成、脂质代谢、胰岛素敏感性和葡萄糖稳态的重要转录介质,它越来越被认为是炎症细胞和心血管疾病(CVD)如高血压、心肌肥厚、充血性心力衰竭和动脉粥样硬化的关键因素。PPAR-γ激动剂,即噻唑烷二酮类(TZDs),可增加胰岛素敏感性、降低血糖、减少循环游离脂肪酸和甘油三酯、降低血压、降低炎症标志物,并减少胰岛素抵抗患者和动物模型的动脉粥样硬化。对 PPAR-γ的人类遗传研究表明,该核受体的功能变化与 CVD 有关。最近有争议的临床研究提出了 PPAR-γ 激动剂对心血管系统产生有害作用的问题。这些代谢反应因素与心血管疾病的复杂相互作用有望成为未来的重点关注领域。