Redox homeostasis in cancer and cardiovascular diseases

癌症和心血管疾病中的氧化还原稳态

• 批准号: 9339275
• 负责人: PAUL M. HWANG
• 金额: $ 67.59万
• 依托单位: NATIONAL HEART, LUNG, AND BLOOD INSTITUTE
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/9339275
• 关键词: Affect; Biological; Biology; Cardiovascular Diseases; Cardiovascular system; DNA Damage; Disease; Energy Metabolism; Generations; Genetic; Genomic DNA; Homeostasis; Malignant Neoplasms; Methods; Oxidation-Reduction; Oxidative Stress; Oxygen; Pathogenesis; Reactive Oxygen Species; Stress; mitochondrial dysfunction; neoplastic cell; tumorigenesis

Our previous studies have suggested that mitochondrial dysfunction causes oxidative genomic DNA damage and contributes to tumorigenesis. A major contributing factor is ambient oxygen which is the essential substrate for reactive oxygen species generation that can cause biological damage. Environmental and genetic methods will be used to modulate redox homeostasis and to determine their effect on energy metabolism, tumorigenesis, and cardiovascular disease. We are examining adaptive mechanisms by which cells of neoplastic or cardiovascular origin survive under oxidative or other toxic stress conditions.

我们以前的研究表明，线粒体功能障碍导致氧化基因组DNA损伤，并有助于肿瘤的发生。 一个主要的影响因素是环境氧，它是产生可导致生物损伤的活性氧的基本基质。 环境和遗传方法将用于调节氧化还原稳态，并确定其对能量代谢，肿瘤发生和心血管疾病的影响。 我们正在研究肿瘤或心血管起源的细胞在氧化或其他毒性应激条件下生存的适应机制。