肺动脉平滑肌细胞（PASMCs）增殖和凋亡失衡可导致肺血管重塑，在缺氧性肺动脉高压（HPH）进程中发挥重要作用，ALDH2与细胞增殖和迁移关系密切。我们前期研究发现，ALDH2的活化可调控双孔钾通道TASK-1，减轻缺氧性肺血管重塑，提示ALDH2对HPH有保护作用。预实验还发现，HPH大鼠肺血管组织中TASK-1表达降低，活化的T细胞核因子（NFATc）表达增加。因此，我们提出假设：ALDH2可能通过影响NFATc的表达而调控双孔钾通道TASK-1，进而逆转HPH的肺血管重塑。本项目拟采用大鼠HPH模型，观察ALDH2对HPH大鼠血流动力学、右心室指数、肺血管重塑等影响，进一步探讨ALDH2在HPH促进细胞凋亡、对抗肺血管重塑、及对TASK-1通道调控的具体机制；并应用腺相关病毒载体高表达ALDH2靶向治疗大鼠HPH，为ALDH2应用于HPH的防治提供理论基础和实验依据。

Imbalance of pulmonary artery smooth muscle cell proliferation and apoptosis can lead to pulmonary vascular remodeling, which plays an important role in the process of hypoxic pulmonary hypertension (HPH).Our previous studies have found that the activation of mitochondrial ALDH2 can regulate dual-pore potassium channel TASK-1 and reduce oxygen-deficient pulmonary vascular remodeling, suggesting that ALDH2 has a protective effect on HPH.Preliminary experiments also found that TASK-1 expression was decreased in pulmonary vascular tissues of HPH rats, while the expression of activated T nuclear factor (NFATc) was increased.Therefore, we hypothesized that ALDH2 may regulate dual-pore potassium channel TASK-1 by affecting the expression of NFATc, thereby reversing the pulmonary vascular remodeling of HPH.This project intends to use rat HPH model to observe the influence of ALDH2 on hemodynamics, right ventricular index and pulmonary vascular remodeling in HPH rats, and further explore the specific mechanism of ALDH2 in promoting apoptosis, fighting pulmonary vascular remodeling and regulating TASK-1 channel in HPH.In addition, adeno-associated virus vector with high expression of ALDH2 was applied to target treatment of rat HPH, providing theoretical basis and experimental basis for the application of ALDH2 in the prevention and treatment of HPH.