Our laboratory has been focusing on the mechanisms of fibrosis elucidating the links between activation of redox pathways, cell death, stellate cell activation and transdifferentiation to myofibroblasts. We have been interested in the role of NADPH oxidases and their cell-specific roles in liver injury and repair. We are investigating how changes in the mechanical properties of the extracellular matrix and architecture elicit changes in cellular behavior, and how these predispose to cancer invasion. While matrix stiffness in advanced fibrosis/cirrhosis and its effects on cancer progression have been extensively studied, we demonstrated how changes in viscoelasticity, independent of stiffness, impact hepatocellular carcinoma growth. This is clinically very relevant as increasing viscoelasticity could be a new risk factor foretelling more invasive features of cancer in diabetic patients.
With the type 2 diabetes and steatotic liver disease epidemics, the ultimate goal is to translate our findings and develop novel therapeutic approaches that improve patient outcomes.