Vascular inflammation plays an important role in the development and progression of cardiovascular diseases, such as atherosclerosis and diabetic vascular complications. Recently, we identified two key molecules, namely orphan nuclear receptor Nur77 and Protein-L-isoaspartate O-methyltransferase (PIMT), in vascular endothelial cells that have been shown to play a key role in vascular inflammation, endothelial barrier dysfunction, and vascular ageing. We are seeking to understand how they regulate endothelial hemostasis and barrier dysfunction and to develop novel strategies to improve endothelial function or barrier integrity to combat cardiovascular diseases, such as atherosclerosis, restenosis, and acute lung injury. 

Endothelial cells (ECs) that line blood vessels are constantly exposed to two types of shear stress: unidirectional laminar shear stress (LSS) and oscillatory shear stress (OSS). LSS has been shown to attenuate vascular inflammation, platelet activation, and endothelial barrier dysfunction, whereas OSS exerts the opposite effects. Dr. Sun’s lab has identified a novel gene, namely Latexin that has been shown to play a key role in this process. Recent findings from Dr. Sun’s laboratory have demonstrated that Latexin is a key player in regulating vascular permeability, smooth muscle cell proliferation, and platelet function. Presently, Dr. Sun’s lab has successfully developed several genetic tools and Latexin inhibitory agents to determine whether targeting Latexin is effective for the treatment of atherothrombosis, acute lung injury, and abdominal aortic aneurysm in various preclinical models of cardiovascular diseases.