Huan Tao, MD, PhD
Research Assistant Professor of Medicine
Dr. Tao’s research interests focus on lipoproteins and macrophages in atherosclerosis. The deposition of lipid-filled macrophages (foam cells) and the activation of inflammatory responses in the arterial wall are hallmarks of atherosclerosis. Increased LDL and less or dysfunctional HDL are major risk factors of atherosclerosis. His studies concentrate on macrophage genes involved in cholesterol homeostasis, inflammation, efferocytosis, and survival. Currently, he is working on two projects: (1) The roles and mechanisms of scavenger receptor SR-BI and apolipoprotein E in atherosclerosis and (2) dysfunctional HDL in human familial hypercholesterolemia (FH). His studies reveal that macrophage SR-BI regulates inflammation, apoptosis, and efferocytosis in atherosclerotic lesion via Src/PI3K/Rac1 signaling and reduces atherosclerotic lesion necrosis. His research has also identified macrophage GSTP1 as a novel SR-BI interacting protein, demonstrating that macrophage SR-BI recognizes oxidized lipid for clearance via a GSTP1 detoxification pathway, thus limiting cell apoptosis and inflammation in atherosclerotic plaques. Additionally, he and his colleagues have recently identified a novel function of macrophage SR-BI, suggesting that the loss of SR-BI-mediated macrophage autophagy and angiogenin-induced tRNA-derived RNA cellular homeostasis promotes the development of atherosclerosis. Finally, his studies find that compared to healthy control HDL, FH HDL is impaired in promoting cholesterol efflux and in preventing inflammation. The HDL dysfunction is likely the result of oxidative modification as a-tocopherol improves HDL function and FH versus control HDL, which contains more isoketal- and malondialdehyde (MDA)-lysyl adducts. ApoA1 from FH patients shows MDA adducts. Using an LDLR-/- mouse FH model, Dr. Tao has shown that salicylamine (aldehyde scavenger) treatment significantly suppresses atherosclerosis.