Stroke is a leading cause of mortality worldwide. One of the most important etiologies of stroke is large artery atherosclerosis and genetics play an important role in the initiation and progression of atherosclerosis. Therefore, a deeper understanding of genetics that affecting atherosclerosis may lead to novel prevention and therapeutic strategies.
Several transcription factors have been identified to be associated with atherosclerosis, such as NF-kB, Krüppel-like factors, BACH1, etc. Those transcription factors modulate the activation of inflammatory mediators, thereby promoting the pathogenesis of atherosclerosis. Prior studies have characterized the role of transcription factors in rodent models, whereas the validation of the relationship between transcription factors and atherosclerosis in human is limited due to many reasons.
This project aims to systematically investigate the associations of genetic, hemodynamic profiles, as well as external environmental exposures with development of large artery atherosclerosis (carotid atherosclerosis, etc.) based on human biomedical data. The genetic heterozygosity of transcription factors established by animal models and their relationships with large artery atherosclerosis as well as ischemic strokes will be the main focus of this project. Leveraging population-level data from the UK Biobank, this project will contribute to novel insights into the identification of potential prevention and/or therapeutic targets for atherosclerosis.