Bio
Our primary research interest is in the pathomechanisms of liver fibrosis and matrix remodeling, and their role in the development of hepatocellular carcinoma.
Clinically, metabolic dysfunction associated steatohepatitis (MASH) is becoming the leading cause of chronic liver disease and liver cancer, and we are interested in deciphering how dynamic changes in the liver matrix accelerate this process in certain conditions such as type 2 diabetes. Of particular interest are studies on collagen architecture and connectivity and how these are implicated in mechanosensing. We are also focusing on aging-related pathways and wound healing processes. We are exploring the age-related modulation of hepatocyte stress signals, metabolic changes, and how these intersect with innate immune responses and matrix modulation in the liver. Based on these studies we have identified targets for novel small molecule inhibitors to treat fibrosis, and are performing investigator-initiated clinical trials.
As MASH is becoming the most common liver disease in the US and worldwide our ultimate goal is to target high-risk populations, and to develop novel therapeutic approaches that reverse fibrosis and improve patient outcomes.