Oxidative stress signalling and lipid metabolism in lifespan regulation (B01)

寿命调节中的氧化应激信号和脂质代谢（B01）

• 批准号: 318028141
• 金额: --
• 依托单位: Institut für Mitochondriale Alterung & Erkrankung (AG Trifunovic)
• 依托单位国家: 德国
• 项目类别: Collaborative Research Centres
• 财政年份: 2016
• 资助国家: 德国
• 起止时间: 2015-12-31 至 2023-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/318028141?language=en
• 关键词: Oxidative; stress; signalling; lipid; metabolism

Increasing body of evidence indicate that at moderate concentrations, ROS acts as a second messenger that regulates a number of signalling pathways. We identified a redox-regulated transcription factor KLF-1 as a mediator of a cytoprotective response that dictates longevity induced by reduced mitochondrial function. In particular we identified KLF-1 mediated regulation of peroxisomal lipid metabolism as essential for longevity assurance in mitochondrial that we intend to address in the second funding period.

越来越多的证据表明，在中等浓度下，ROS 充当调节许多信号通路的第二信使。我们确定了一种氧化还原调节转录因子 KLF-1 作为细胞保护反应的介体，该反应决定了线粒体功能减少诱导的寿命。特别是，我们发现 KLF-1 介导的过氧化物酶体脂质代谢调节对于线粒体的长寿保证至关重要，我们打算在第二个资助期解决这一问题。