Research Background:
Cardiovascular diseases (CVDs)-including coronary artery disease, stroke, peripheral vascular disease, heart failure, and selected arrhythmias-remain leading causes of morbidity and mortality worldwide. These conditions arise from interconnected biological processes involving endothelial dysfunction, vascular remodeling, lipid and glucose metabolic dysregulation, oxidative stress, chronic inflammation, and immune imbalance. Major, well-established risk factors-including hypertension, dyslipidemia, obesity, diabetes, smoking, and physical inactivity-interact with genetic susceptibility, molecular perturbations, environmental exposures, and behavioral factors to determine individual risk and disease trajectories.
Aims and Objectives:
1.Identify genetic variants and circulating multi-omics biomarkers associated with CVDs onset, progression, and prognosis.
2.Integrate genomic, proteomic, metabolomic, and imaging-derived phenotypes to reveal key biological pathways and population-level heterogeneity.
3.Assess the causal impact of modifiable lifestyle and environmental exposures on CVDs risk and outcomes.
4.Characterize multimorbidity patterns and shared molecular mechanisms linking CVDs with other chronic conditions such as metabolic syndrome, cognitive decline, and cancer.
Scientific rationale:
CVDs arise from interacting processes-endothelial dysfunction, vascular remodeling, metabolic dysregulation, oxidative stress, chronic inflammation, and immune dysregulation by genetic susceptibility and environmental and behavioral exposures. Integrative multi-omics and imaging analyses can reveal early molecular and structural changes, improve risk stratification beyond traditional factors, and identify modifiable pathways for prevention. Leveraging multidimensional UK Biobank data, we will build predictive models, infer causality, and identify intervention targets to inform precision prevention and public strategies for reducing CVD burden.
