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.

中文翻译：

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Galectin-3在缺氧诱导的肺动脉高压中介导肺血管重构。

肺血管外膜在肺动脉高压（PAH）的发病机理中起着关键的调节作用。肺外膜成纤维细胞（PAFs）的过度增殖和分化被证明在PAH的发病机理中至关重要。Galectin-3（Gal-3）是关键的成纤维细胞活化因子，它参与多种疾病的纤维化，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PAF发病机理中对PAF细胞的潜在作用。在PAH患者中，Gal-3血浆浓度显着较高。Gal-3在缺氧诱导的PAH大鼠的肺动脉外膜上调。N-乙酰基-D-乳糖胺（N-Lac）抑制Gal-3可改善PAH和肺血管重构。Gal-3可以刺激PAF的增殖，分化和胶原蛋白合成，而N-Lac可以逆转它。转化生长因子β1增加PAF中Gal-3的表达，而N-Lac显着抑制转化生长因子β1诱导的PAF增殖，分化和胶原合成。Gal-3通过调节PAF的增殖，分化和细胞外基质沉积合成，在PAH的发病机理中起着至关重要的调节作用。Gal-3的抑制可能代表PAH治疗的新型治疗靶点。和PAFs的胶原合成。Gal-3通过调节PAF的增殖，分化和细胞外基质沉积合成，在PAH的发病机理中起着至关重要的调节作用。Gal-3的抑制可能代表PAH治疗的新型治疗靶点。和PAFs的胶原合成。Gal-3通过调节PAF的增殖，分化和细胞外基质沉积合成，在PAH的发病机理中起着至关重要的调节作用。Gal-3的抑制可能代表PAH治疗的新型治疗靶点。