Role and potential for therapeutic targeting of dysfunction, oxidative stress and altered metabolism in mitochondria in the pathogenesis of COPD

线粒体功能障碍、氧化应激和代谢改变在慢性阻塞性肺病发病机制中的作用和潜力

• 批准号: nhmrc : GNT1099095
• 负责人: Prof Ian Adcock
• 金额: $ 72.03万
• 依托单位: University of Technology Sydney
• 依托单位国家: 澳大利亚
• 项目类别: Project Grants
• 财政年份: 2016
• 资助国家: 澳大利亚
• 起止时间: 2016-01-01 至 无数据
• 项目状态: 已结题
• 来源: https://researchdata.edu.au/role-potential-therapeutic-pathogenesis-copd/1346031
• 关键词: Role; potential; therapeutic; targeting; dysfunction

Emphysema is a major cause of illness and death and there are no good treatments. It is caused by smoking that induces lung inflammation and disease but how this occurs is not well understood. Cellular respiration can become defective causing oxidative stress, altered metabolism and inflammation. We think that this drives emphysema. We will assess alterations in respiration, oxidative stress and metabolism in emphysema and see if we can reverse these changes with new potential treatments.

肺气肿是疾病和死亡的主要原因，没有很好的治疗方法。它是由吸烟引起的，导致肺部炎症和疾病，但这是如何发生的还不清楚。细胞呼吸可能会变得有缺陷，导致氧化应激，代谢改变和炎症。我们认为这会导致肺气肿。我们将评估肺气肿中呼吸、氧化应激和代谢的变化，看看我们是否可以用新的潜在治疗方法逆转这些变化。