Hi and welcome to my website!
I’m Daisy Shu, a PhD candidate at the Lens Research Laboratory at the University of Sydney.
My research interest involves unravelling the cellular and molecular mechanisms involved in ocular wound healing. My aim is to explore how excessive and aberrant wound healing results in scar formation and subsequently drives the formation of fibrotic eye diseases. My area of expertise is in growth factor signalling pathways, in particular the signalling pathways downstream of transforming growth factor-beta. As multicellular organisms, maintaining the function of our cells involves coordinated cell-to-cell communication through signalling proteins. Using molecular biology techniques analysing protein and gene expression, my research seeks to eavesdrop on the cellular conversation mediating the wound healing response.
My PhD project (supervised by Professors Frank Lovicu and John McAvoy at the University of Sydney) explores the wound healing mechanisms in lens epithelial cells and the role of transforming growth factor-beta-induced epithelial-mesenchymal transition in cataract formation. By investigating the downstream signalling pathways mediating wound healing, I have discovered novel targets that can be blocked to specifically combat fibrotic cataract.
From January-March 2018, I collaborated on a project with Professor Andrew White at the Westmead Institute for Medical Research exploring the wound healing mechanisms following glaucoma filtration surgery. The most critical determinant of the success of glaucoma surgery is scar formation and by understanding the signalling pathways involved in scarring, novel anti-fibrotic agents can be developed to maximize the surgical success of glaucoma filtration surgery.
Currently, I am in Boston, MA collaborating on a project with Professor James Zieske at Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School under the supervision of Dr Xiaoqing Guo and Audrey Hutcheon on wound healing mechanisms in the cornea by exploring the interplay between TGF-beta and EGF signaling cascades.