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过氧化物酶体增殖物激活受体β/δ激动剂 GW0742 对右心肥厚有直接的保护作用。

The peroxisome proliferator-activated receptor β/δ agonist GW0742 has direct protective effects on right heart hypertrophy.

机构信息

Universities of Giessen and Marburg Lung Center, Giessen, Germany.

Cardiothoracic Pharmacology, National Heart and Lung Institute, Imperial College, London, United Kingdom.

出版信息

Pulm Circ. 2013 Dec;3(4):926-35. doi: 10.1086/674755.

Abstract

Pulmonary hypertension is a debilitating disease with no cure. We have previously shown that peroxisome proliferator-activated receptor (PPAR) β/δ agonists protect the right heart in hypoxia-driven pulmonary hypertension without affecting vascular remodeling. PPARβ/δ is an important receptor in lipid metabolism, athletic performance, and the sensing of prostacyclin. Treatment of right heart hypertrophy and failure in pulmonary hypertension is an emerging target for future therapy. Here we have investigated the potential of GW0742, a PPARβ agonist, to act directly on the right heart in vivo and what transcriptomic signatures are associated with its actions. Right heart hypertrophy and failure was induced in mice using a pulmonary artery banding (PAB) model. GW0742 was administered throughout the study. Cardiovascular parameters were measured using echocardiography and pressure monitoring. Fibrosis and cellular changes were measured using immunohistochemistry. Transcriptomics were measured using the Illumina MouseRef-8v3 BeadChip array and analyzed using GeneSpring GX (ver. 11.0). PAB resulted in right heart hypertrophy and failure and in increased fibrosis. GW0742 reduced or prevented the effects of PAB on all parameters measured. GW0742 altered a number of genes in the transcriptome, with Angptl4 emerging as the top gene altered (increased) in animals with PAB. In conclusion, the PPARβ/δ agonist GW0742 has direct protective effects on the right heart in vivo. These observations identify PPARβ/δ as a viable therapeutic target to treat pulmonary hypertension that may complement current and future vasodilator drugs.

摘要

肺动脉高压是一种无法治愈的使人虚弱的疾病。我们之前已经表明,过氧化物酶体增殖物激活受体(PPAR)β/δ 激动剂在不影响血管重塑的情况下保护缺氧驱动的肺动脉高压中的右心。PPARβ/δ 是脂质代谢、运动表现和前列环素感应的重要受体。肺动脉高压中右心肥大和衰竭的治疗是未来治疗的一个新兴靶点。在这里,我们研究了 PPARβ 激动剂 GW0742 在体内直接作用于右心的潜力,以及与其作用相关的转录组特征。使用肺动脉结扎(PAB)模型在小鼠中诱导右心肥大和衰竭。GW0742 在整个研究过程中给药。使用超声心动图和压力监测测量心血管参数。使用免疫组织化学测量纤维化和细胞变化。使用 Illumina MouseRef-8v3 BeadChip 阵列测量转录组,并使用 GeneSpring GX(版本 11.0)进行分析。PAB 导致右心肥大和衰竭以及纤维化增加。GW0742 减轻或预防了 PAB 对所有测量参数的影响。GW0742 改变了转录组中的许多基因,其中 Angptl4 是 PAB 动物中改变(增加)最多的基因。总之,PPARβ/δ 激动剂 GW0742 对体内右心具有直接的保护作用。这些观察结果表明,PPARβ/δ 是一种可行的治疗肺动脉高压的治疗靶点,可能补充当前和未来的血管扩张药物。

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