Chronic liver diseases (CLD) are diseases of long duration and slow progression and represent a major public health issue. Hepatic fibrosis and cirrhosis are the final outcomes of CLD and have been associated with hepatitis B and C viral infection, alcohol drinking, and non-alcoholic fatty liver disease including non-alcoholic steatohepatitis. More recently, environmental pollutants have been reported to exacerbe liver diseases, and growing impact of CLD in industrialized countries has pointed out the role of occupational lifestyle and environmental pollution in promoting these pathologies.
Understanding the cellular and molecular mechanisms involved in the evolution of CLD is a prerequisite to develop efficient therapeutic approaches. CLDs are characterized by extensive reorganization of the extracellular matrix (ECM) that results in a change in biochemical composition and mechanical properties. Our research aims to understand how this reorganization of the ECM affects liver cell functionality, cell communication, signaling, and response to environmental contaminants.
In this context, our team is developing new strategies based on multi-scale approaches combining molecular and cellular biology, environmental contaminant toxicology, biophysical methods and modeling, to identify exposure markers, signatures and therapeutic targets of fibrosis.