Cardiovascular disease (CVD) remains the predominant cause of global mortality, with atherosclerosis-driven complications representing the primary etiology. Atherosclerosis is characterized by the progressive accumulation of lipids and cholesterol within the arterial wall, leading to plaque formation, rupture, and subsequent thrombotic complications including myocardial infarction and stroke. Established risk factors include smoking, hypertension, diabetes, obesity, hypercholesterolemia, and age-related clonal hematopoiesis of indeterminate potential (CHIP). While current frontline therapies (e.g., statins, PCSK9 inhibitors) reduce plasma LDL levels, they only lower cardiovascular events by <50%, even when LDL is controlled below guidelines. This residual CVD risk is linked to unresolved inflammation, though the mechanisms remain unclear.

Using genetic mouse models, our team collaborates on projects to:

1.Dissect the inter-organ crosstalk mechanisms linking hepatic dyslipidemia to myocardial dysfunction.

2.Define CHIP-driven inflammatory mechanisms in atherosclerosis.

3.Develop novel lineage-tracing mice to study cellular clonal expansion.

 

The overarching goal of our group is to identify novel therapeutic targets with translational potential to improve clinical outcomes in CVD patients.