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本文引用的文献

1
Rosiglitazone attenuates chronic hypoxia-induced pulmonary hypertension in a mouse model.罗格列酮可减轻小鼠慢性低氧性肺动脉高压。
Am J Respir Cell Mol Biol. 2010 Apr;42(4):482-90. doi: 10.1165/rcmb.2008-0132OC. Epub 2009 Jun 11.
2
Pulmonary arterial hypertension is linked to insulin resistance and reversed by peroxisome proliferator-activated receptor-gamma activation.肺动脉高压与胰岛素抵抗相关,而过氧化物酶体增殖物激活受体γ激活可逆转这种关系。
Circulation. 2007 Mar 13;115(10):1275-84. doi: 10.1161/CIRCULATIONAHA.106.663120. Epub 2007 Mar 5.
3
The PPARgamma ligand, rosiglitazone, reduces vascular oxidative stress and NADPH oxidase expression in diabetic mice.过氧化物酶体增殖物激活受体γ(PPARγ)配体罗格列酮可降低糖尿病小鼠的血管氧化应激及NADPH氧化酶表达。
Vascul Pharmacol. 2007 Jun;46(6):456-62. doi: 10.1016/j.vph.2007.01.007. Epub 2007 Feb 8.
4
Rosiglitazone attenuates hypoxia-induced pulmonary arterial remodeling.罗格列酮可减轻缺氧诱导的肺动脉重塑。
Am J Physiol Lung Cell Mol Physiol. 2007 Apr;292(4):L885-97. doi: 10.1152/ajplung.00258.2006. Epub 2006 Dec 22.
5
Peroxisome proliferator-activated receptor-gamma activation with pioglitazone improves endothelium-dependent dilation in nondiabetic patients with major cardiovascular risk factors.吡格列酮激活过氧化物酶体增殖物激活受体γ可改善伴有主要心血管危险因素的非糖尿病患者的内皮依赖性血管舒张功能。
Circulation. 2006 Feb 14;113(6):867-75. doi: 10.1161/CIRCULATIONAHA.105.549618. Epub 2006 Feb 6.
6
Chronic ethanol exposure stimulates endothelial cell nitric oxide production through PI-3 kinase-and hsp90-dependent mechanisms.长期乙醇暴露通过PI-3激酶和热休克蛋白90依赖性机制刺激内皮细胞一氧化氮生成。
Alcohol Clin Exp Res. 2005 Nov;29(11):1932-8. doi: 10.1097/01.alc.0000187597.62590.a4.
7
Pulmonary hypertension surveillance--United States, 1980-2002.1980 - 2002年美国肺动脉高压监测
MMWR Surveill Summ. 2005 Nov 11;54(5):1-28.
8
Peroxisome proliferator-activated receptor gamma ligands stimulate endothelial nitric oxide production through distinct peroxisome proliferator-activated receptor gamma-dependent mechanisms.过氧化物酶体增殖物激活受体γ配体通过不同的过氧化物酶体增殖物激活受体γ依赖性机制刺激内皮细胞一氧化氮生成。
Arterioscler Thromb Vasc Biol. 2005 Sep;25(9):1810-6. doi: 10.1161/01.ATV.0000177805.65864.d4. Epub 2005 Jul 14.
9
[Effects of peroxisome proliferator-activated receptor gamma ligands on monocrotaline-induced pulmonary hypertension in rats].过氧化物酶体增殖物激活受体γ配体对野百合碱诱导的大鼠肺动脉高压的影响
Nihon Kokyuki Gakkai Zasshi. 2005 May;43(5):283-8.
10
Peroxisome proliferator-activated receptor-gamma ligands regulate endothelial membrane superoxide production.过氧化物酶体增殖物激活受体γ配体调节内皮细胞膜超氧化物的产生。
Am J Physiol Cell Physiol. 2005 Apr;288(4):C899-905. doi: 10.1152/ajpcell.00474.2004. Epub 2004 Dec 8.

过氧化物酶体增殖物激活受体γ在肺血管疾病中的作用。

The Role of PPARgamma in pulmonary vascular disease.

作者信息

Hart C Michael

机构信息

Atlanta Veterans Affairs Medical Center, Atlanta, GA, USA.

出版信息

J Investig Med. 2008 Feb;56(2):518-21. doi: 10.2310/JIM.0b013e318165e921.

DOI:10.2310/JIM.0b013e318165e921
PMID:18317434
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4484596/
Abstract

The peroxisome proliferator-activated receptor (PPAR) gamma is a member of the nuclear hormone receptor superfamily of ligand-activated transcription factors. Thiazolidinediones, pharmacological ligands for PPARgamma, are currently used in the management of type 2 diabetes. Peroxisome proliferator-activated receptor gamma is expressed in the lung and pulmonary vasculature, and its expression is reduced in the vascular lesions of patients with pulmonary hypertension. Furthermore, thiazolidinedione PPARgamma ligands reduced pulmonary hypertension and vascular remodeling in several experimental models of pulmonary hypertension. This report reviews current evidence that PPARgamma may represent a novel therapeutic target in pulmonary hypertension and examines studies that have begun to elucidate mechanisms that underlie these potential therapeutic effects.

摘要

过氧化物酶体增殖物激活受体(PPAR)γ是配体激活转录因子核激素受体超家族的成员。噻唑烷二酮类药物是PPARγ的药理学配体,目前用于2型糖尿病的治疗。过氧化物酶体增殖物激活受体γ在肺和肺血管系统中表达,在肺动脉高压患者的血管病变中其表达降低。此外,噻唑烷二酮类PPARγ配体在几种肺动脉高压实验模型中降低了肺动脉高压和血管重塑。本报告综述了目前关于PPARγ可能是肺动脉高压新治疗靶点的证据,并审视了已开始阐明这些潜在治疗作用机制的研究。