Our group investigates the molecular and cellular mechanisms underlying stress- and disease-induced cardiovascular remodeling. More specifically, our work focuses on macrophage function in ischemia/reperfusion-triggered heart failure, Sepsis-caused cardiovascular leakage, Diabetes-induced microvascular rarefaction and cardiac dysfunction. The lab uses in vivo transgenic and knockout animal models as well as in vitro primary cell culture to identify and validate novel therapeutic targets in cardiovascular disease. In addition, multiple state-of-art techniques (i.e., adenovirus-mediated gene transfer, single-cell/bulk RNA sequencing, cell sorting, flow cytometry, Co-IP, co-immunostaining, and bioinformatics) are employed to analyze the associated molecular/cellular mechanisms.
Among possible lines of investigations, we chose to focus primarily on macrophage-associated proteins (i.e., Sectm1a, Lcn10) and extracellular membrane vesicles (collected from mammalian cells or gut bacteria) in the regulation of macrophage phagocytosis, efferocytosis and polarization, endothelial permeability and cardiac contractile function, because both acute and long-term inflammation are major culprits to cardiovascular disease, which are outlined below.
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