Emerging evidence suggests that immune dysregulation contributes to cardiovascular disease not only through local inflammatory processes within the heart and vasculature, but also via systemic, immune-mediated inter-organ communication involving the liver, spleen, adipose tissue, lung, kidney, and other immune-relevant organs. However, the mechanisms through which these multi-organ immune interactions shape cardiovascular disease progression, structural remodeling, and therapeutic outcomes remain poorly understood.
This study seeks to investigate how systemic immune phenotypes and immune-driven inter-organ crosstalk contribute to cardiovascular pathology, with a particular focus on cardiac fibrosis, vascular fibrosis, and vascular remodeling. The study will also explore how genetic variation modulates immune-mediated communication between the heart, vasculature, and peripheral organs such as the liver, spleen, kidney, lung, and adipose tissue, and whether genetically regulated immune pathways shaping this inter-organ network contribute to inter-individual differences in cardiovascular risk and disease trajectories. Furthermore, it will assess the extent to which baseline and dynamic immune states influence therapeutic response, disease regression, or continued progression, thereby identifying immune profiles that predict treatment efficacy, resistance, or adverse outcomes.
By integrating immune phenotypes with genetic information, multi-omics biomarkers, and longitudinal cardiovascular outcomes, this study aims to identify immune-mediated pathways that link immune regulation across organs to cardiovascular disease onset, progression, and heterogeneity.
