| Property | Value |
|
overview
|
My research foci are mechano-transduction mechanisms by which cells sense and convert environmental mechanical stimuli into biological signaling and novel nanomedicine approaches that target dysregulated mechano-sensing pathways. Cellular mechanotransduction is instrumental to embryogenesis and physiological control of tissue homeostasis; abnormal cell responses to mechanical forces promote pathologies associated with numerous human diseases. This is especially important in the vasculature, where environmental mechanical stimuli produce cellular responses in endothelial cells at arterial curvatures and bifurcations by locally disturbed blood flow to induce atherosclerosis. A similar cascade appears to be induced in acute lung injury where it is the increased cyclic stretch that is the trigger. My research program at the University of Chicago focuses on the molecular understanding of endothelial homeostasis governed by mechanical forces, with emphasis upon regulation of non-coding genome, transcription factors, G protein signaling, and genetic variance. Another major research goal is to develop innovative nanomedicine-based therapeutic strategies to treat dysregulated mechano-sensing mechanisms causing vascular diseases.
Key Words: microRNA, non-coding RNA, human genetics, enhancer biology, vascular biology, nanotechnology, nanomedicine, mechanotransduction, atherosclerosis, acute lung injury
|
|
overview
|
Dr. Fang conducts research focused on the mechanisms of mechanotransduction—how cells sense and convert environmental mechanical stimuli into biological signals—and the development of novel nanomedicine approaches targeting dysregulated mechanosensing pathways. Cellular mechanotransduction plays a critical role in embryogenesis and the physiological regulation of tissue homeostasis, while abnormal cellular responses to mechanical forces contribute to a wide range of human diseases.
Dr. Fang’s work is particularly relevant to the vascular system, where mechanical stimuli such as disturbed blood flow at arterial curvatures and bifurcations elicit pathogenic responses in endothelial cells, contributing to the development of atherosclerosis. A similar mechanosensitive cascade is also observed in acute lung injury, where increased cyclic stretch serves as a pathological trigger.
At the University of Chicago, Dr. Fang’s research program is dedicated to uncovering the molecular mechanisms that govern endothelial homeostasis in response to mechanical forces. This includes studying the regulation of the non-coding genome, transcription factors, G protein signaling, and the impact of genetic variation. A major goal of the lab is to translate these insights into innovative nanomedicine-based therapeutic strategies designed to correct dysregulated mechanosensing mechanisms underlying vascular diseases.
|