Effects of redox homeostasis on cancer and cardiovascular diseases

氧化还原稳态对癌症和心血管疾病的影响

• 批准号: 9157381
• 负责人: PAUL M. HWANG
• 金额: $ 59.03万
• 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/9157381
• 关键词: Aerobic; Affect; Biological; Biology; Cardiovascular Diseases; Cardiovascular system; Cell model; Cellular Stress; DNA Damage; Development; Disease; Energy Metabolism; Genetic; Genomic DNA; Health; Homeostasis; Human; Life; Malignant Neoplasms; Methods; Mitochondria; Nuclear; Oxidation-Reduction; Oxygen; Pathogenesis; Reactive Oxygen Species; Stress; mitochondrial dysfunction; mouse model; neoplastic cell; prevent; tumorigenesis

Our previous studies have suggested that mitochondrial dysfunction causes oxidative genomic DNA damage and contributes to tumorigenesis. Oxygen is necessary for aerobic life but it also serves as the essential substrate for reactive oxygen species that can cause biological damage. We are currently using environmental and genetic methods to modulate oxygen homeostasis and to examine their effect on energy metabolism, tumorigenesis, and cardiovascular disease. We are also 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。 氧是有氧生活所必需的，但它也是活性氧的基本基质，可导致生物损伤。 我们目前正在使用环境和遗传的方法来调节氧稳态，并检查其对能量代谢，肿瘤发生和心血管疾病的影响。 我们也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。