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Cardiovascular complications are significant clinical challenges in cardiometabolic diseases such as diabetes and obesity, contributing to high morbidity and mortality worldwide. Despite their prevalence, the underlying mechanisms remain poorly understood, and there is a lack of specific therapies and reliable biomarkers to address cardiovascular injury.

In recent years, our work has revealed that red blood cells (RBCs), traditionally viewed as passive oxygen carriers, undergo dysfunction and act as active mediators of vascular injury. This dysfunction contributes to the development of vascular complications in type 2 diabetes, familial hypercholesterolemia, ST-elevation myocardial infarction, and COVID-19. Targeting these dysfunctional RBCs has emerged as a promising strategy for treating vascular dysfunction.

RBCs are a rich source of diverse non-coding RNAs (ncRNAs). Through high-throughput profiling and functional validation, using samples from well-characterized clinical cohorts and disease models—including genetically modified animals—our team investigates the expression and functional role of RBC-derived ncRNAs. We explore how alterations in these ncRNAs contribute to cardiovascular complications and their potential as biomarkers and therapeutic targets.

Additionally, RBCs function as ATP reservoirs, releasing ATP under physiological conditions. However, this ATP release is impaired in various disease states. A critical focus of our research is understanding the functional interactions between RBCs and the cardiovascular wall, specifically through ATP-mediated purinergic signaling pathways in cardiometabolic diseases.

Our ultimate goal is to identify RBC-derived factors as novel mechanisms driving cardiovascular complications and to establish them as diagnostic markers and therapeutic targets, paving the way for improved clinical outcomes in cardiometabolic diseases.