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首页> 外文期刊>Journal of the American Society of Hypertension : >Galectin-3 mediates pulmonary vascular remodeling in hypoxia-induced pulmonary arterial hypertension
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Galectin-3 mediates pulmonary vascular remodeling in hypoxia-induced pulmonary arterial hypertension

机译：Galectin-3在缺氧诱导的肺动脉高压症中介导肺血管重塑

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Abstract Pulmonary vascular adventitia serves as a key regulator of pulmonary vascular remodeling in the pathogenesis of pulmonary arterial hypertension (PAH). Excessive proliferation and differentiation of pulmonary adventitial fibroblasts (PAFs) are proven to be crucial in the pathogenesis of PAH. Galectin-3 (Gal-3) is known as a key fibroblasts activating factor which is involved in the fibrogenesis of several diseases, such as pulmonary fibrosis, vascular fibrosis, and heart failure. Therefore, we seek to investigate the potential role of Gal-3 in regulating PAF cells in the pathogenesis of PAH. Gal-3 plasma concentration was significantly higher in PAH patients. Gal-3 was upregulated in pulmonary artery adventitia of hypoxia-induced PAH rats. Inhibition of Gal-3 with N-Acetyl-D-lactosamine (N-Lac) ameliorated PAH and pulmonary vascular remodeling. Gal-3 can stimulate the proliferation, differentiation, and collagen synthesis of PAFs, which was reversed by N-Lac. Transforming growth factor β1 increased Gal-3 expression in PAFs, whereas N-Lac significantly suppressed transforming growth factor β1–induced proliferation, differentiation, and collagen synthesis of PAFs. Gal-3 serves as a critical regulator in the pathogenesis of PAH by regulating the proliferation, differentiation, and extracellular matrix deposition synthesis of PAFs. Inhibition of Gal-3 may represent a novel therapeutic target for PAH treatment. Highlights ? Galectin-3 (Gal-3) was upregulated in pulmonary artery adventitia of hypoxia-induced pulmonary arterial hypertension rats, inhibition of Gal-3 ameliorated pulmonary arterial hypertension and pulmonary vascular remodeling. ? Gal-3 can stimulate the proliferation, differentiation, and collagen synthesis of pulmonary adventitial fibroblasts (PAFs), which was reversed by Gal-3 inhibitors. ? Transforming growth factor β1 increased Gal-3 expression in PAFs, whereas inhibition of Gal-3 significantly suppressed transforming growth factor β1 induced PAFs proliferation, differentiation, and collagen synthesis. ]]>
机译：摘要肺血管复位肌瘤用作肺动脉高血压发病机制（PAH）的肺血管重塑的关键调节因子。肺部过度成纤维细胞（PAF）的过度增殖和分化被证明在PAH的发病机制中至关重要。 Galectin-3（GAL-3）被称为键成纤维细胞激活因子，其涉及几种疾病的纤维发生，例如肺纤维化，血管纤维化和心力衰竭。因此，我们寻求研究GAL-3在调节PAH的PAF细胞在PAH的发病机制中的潜在作用。 PAH患者的GAL-3等离子体浓度显着高。 GAL-3在缺氧诱导的PAH大鼠肺动脉外膜上升级。用N-乙酰基-D-乳鞘胺（N-LAC）改善PAH和肺血管重塑的GAL-3对GAL-3的抑制作用。 GAL-3可以刺激PAF的增殖，分化和胶原蛋白合成，其被N-LAC逆转。转化生长因子β1增加PAF中的GAL-3表达，而N-LAC显着抑制了转化生长因子β1诱导的PAFS增殖，分化和胶原蛋白合成。通过调节PAF的增殖，分化和细胞外基质沉积合成，GAL-3作为PAH发病机制中的临界调节剂。 GAL-3的抑制可以代表PAH治疗的新疗法靶标。强调 ？ Galectin-3（Gal-3）在缺氧诱导的肺动脉高压大鼠的肺动脉外膜上进行了上调，抑制GAL-3改善肺动脉高压和肺血管重塑。还GAL-3可以刺激肺部过度成纤维细胞（PAF）的增殖，分化和胶原合成，其被GAL-3抑制剂逆转。还转化生长因子β1增加PAF中的GAL-3表达，而GAL-3的抑制显着抑制了转化生长因子β1诱导的PAFS增殖，分化和胶原合成。 ]]>

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