Research & Publications
Extensive Research Description
My main interest is heart and vascular diseases caused by inflammation. Excessive/chronic inflammatory responses (e.g., TNF) and increases in reactive oxygen species (ROS) represent common pathogenic mechanism for atherosclerosis. The vascular cell that primarily limits the inflammatory and atherosclerotic process is the vascular endothelial cells (EC). Inflammation/ROS induces EC dysfunction by disturbing normal homeostasis, relaxation and survival. These defects in EC function are mediated by cytokine/redox-regulated signal transduction and gene transcription. My experiments are designed to dissect signal pathways during inflammatory responses. We have identified that AIP1 plays important roles inTNF signaling pathways in EC by interacting with ASK1,TRAF2 and RIP1. AIP1's other functions such as tumor suppression are under investigation.