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

血管 NFAT5 对肺功能和缺氧反应的影响 (B05)

• 批准号: 418411994
• 金额: --
• 依托单位: Institut für Physiologie und Pathophysiologie
• 依托单位国家: 德国
• 项目类别: Collaborative Research Centres
• 财政年份: 2019
• 资助国家: 德国
• 起止时间: 2018-12-31 至 2021-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/418411994?language=en
• 关键词: Impact; vascular; NFAT5; lung; function

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.

肺形成用于气体交换的专门边界，并且可以通过调整其灌注以优化血液氧合来快速响应局部缺氧。然而，与许多肺部疾病相关的慢性缺氧促进不可逆的结构重塑和随后的肺功能障碍。我们观察到转录因子NFAT 5在缺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。具体而言，将研究血管转录组的NFAT 5依赖性修饰及其对肺阻力、血氧和肺泡巨噬细胞活化的影响。