Impact of vascular NFAT5 on lung function and responses to hypoxia (B05)

肺形成了气体交换的特殊边界，并可能通过调整其血流以优化血液氧合，对局部缺氧做出快速反应。然而，与许多肺部疾病相关的慢性缺氧会促进不可逆转的结构重建和随后的肺功能障碍。我们观察到转录因子NFAT5在低氧肺的血管内皮细胞和平滑肌细胞中表达，并试图研究其在控制结构重塑和炎症反应中的作用。具体地说，将研究依赖于NFAT5的血管转录组的修饰及其对肺阻力、血液氧合和肺泡巨噬细胞激活的影响。

The lung forms a specialized border for gas exchange and may rapidly respond to local hypoxia by adapting its perfusion for optimized blood oxygenation. However, chronic hypoxia that is associated with many pulmonary diseases promotes irreversible structural remodeling and subsequent lung dysfunction. We observed that the transcription factor NFAT5 is expressed in vascular endothelial and smooth muscle cells of the hypoxic lung and seek to study its role in controlling structural remodeling and inflammatory responses. Specifically, the NFAT5-dependent modification of the vascular transcriptome and its impact on pulmonary resistance, blood oxygenation and activation of alveolar macrophages will be investigated.