The role of inflammation in pulmonary hypertension is gradually gaining increasing research attention. However, no previous study has evaluated the characteristics of inflammation during chronic hypoxia-induced pulmonary hypertension. Therefore, the aim of this study was to investigate the characteristics of the inflammatory process involved in hypoxia-induced pulmonary hypertension in mice. The current study evaluated from day 4 to day 28 of hypoxia, the PAAT and PAAT/PET decreased, accompanied by pulmonary vascular remodeling and right ventricular hypertrophy, as well as increased numbers of CD68 macrophages. The expression of the pro-inflammatory factors IL-1β and IL-33 increased, but decreased on day 28. The expression of IL-12 increased from day 4 to day 28, whereas that of the anti-inflammatory factor IL-10 in lung tissue decreased. Furthermore, the expression of the IL-33/ST2 signaling pathway also increased over time under hypoxic conditions. In conclusion, pulmonary artery remodeling in HPH mice worsens progressively in a time-dependent manner, with inflammatory cell infiltration predominating in the early stage and pulmonary vascular remodeling occurring in the later stage.

炎症在肺动脉高压中的作用逐渐受到越来越多的研究关注。然而，先前的研究尚未评估慢性缺氧引起的肺动脉高压期间的炎症特征。因此，本研究的目的是探讨小鼠缺氧性肺动脉高压所涉及的炎症过程的特征。本研究评估缺氧第4天至第28天，PAAT和PAAT/PET下降，伴有肺血管重塑和右心室肥厚，以及CD68巨噬细胞数量增加。肺组织中促炎因子IL-1β和IL-33的表达增加，但在第28天下降。IL-12的表达从第4天到第28天增加，而抗炎因子IL-10的表达在第4天至第28天增加。组织减少。此外，在低氧条件下，IL-33/ST2信号通路的表达也随着时间的推移而增加。总之，HPH小鼠的肺动脉重塑呈时间依赖性进行性恶化，早期以炎症细胞浸润为主，后期发生肺血管重塑。