Bond Lab Research

Research Interests

Our work on cAMP highlighted the central role of actin cytoskeleton remodelling in integrating multiple upstream signals and regulating appropriate cellular responses. This prompted us to investigate how biomechanical signals also feed into common downstream pathways and how cells process the multitude of signals coming in from the extracellular environment, and decide how to modulate their phenotype. Our current research is focussing on how these mechanisms are involved in regulating cell behaviour during a number of pathological processes that underly cardiovascular disease. These include sensing changes in cardiac and arterial tissue stiffness and regulating cardiac fibrosis and VSMC phenotypic modulation. How actin monomers can translocate into the nucleus and control expression of genes that regulate these processes remains an important focus of our research.

Investigating the mechanosensitive and cAMP-sensitive transcription factors led us to identify a key role for YAP-TEAD and NFY transcription factors in driving cell hyperplasia and fibrosis. In vascular smooth muscle cells, we have identified novel mechanosensitive mechanisms that prime these cells to respond to pro-inflammatory signals. Using molecular docking we have identified small molecule inhibitors of these transcription factors and shown that they work to selectively block gene expression changes induced by a pathologically stiffened ECM.

Please have a look at the Bond Lab publications page to read more about our research.