About
aim: Mitochondria is the essential organelle for many aspects of cellular homeostasis. Mitochondrial dysfunction occurs early and acts causally in disease pathogenesis. It could elicit the inordinate production of ROS, causing macromolecule injury, concurrent with deficits in energy supply and in the production of essential molecules and abnormal mitochondrial signaling transduction. Mitochondrial dysfunction serves as central to the progression of cardiometabolic disorders. More than 90% of the ATP consumed by the heart is derived from mitochondrial oxidative metabolism. Mutations in mitochondrial DNA and oxidative stress both affect mitochondrial function and metabolism, and the mitochondrial genetic variation underlying most cardiovascular metabolic disorders remains unidentified. In the last decade, there are no large sample studies to clarify the mitochondrial DNA genetic variant loci that increase susceptibility to CVDs. Our aim is to investigate whether mitochondrial genetic variants modified the association between unhealthy lifestyle factors and cardiometabolic burden and poor prognosis. There is no large-scale study to assess the mitochondrial DNA variant loci that increase the susceptibility to CVDs. The study may demonstrate the interaction between mitochondrial genetic variants and modifiable risk factors on cardiometabolic burden.
Project duration: 36 months
Public health impact: This project is expected to improve understanding of the interaction of mitochondrial genetic with modifiable lifestyle factors on the cardiometabolic burden and life expectancy, and therefore contribute to guide early individualized management for lifestyle, dietary and environmental risk factors.