Liver diseases are a major burden on human health. In particular, modern lifestyles, including excessive food and alcohol consumptions, are responsible for an ever-increasing number of liver failures and cancers.

Liver diseases are caused by alterations in the activities of hepatocytes, the main cell type that makes up this organ. Indeed, a dysfunctional liver is characterized by unhealthy hepatocytes, unable to maintain normal homeostatic functions. Alterations to hepatocyte functions are accompanied by changes in the activities of other liver cell types, including hepatic stellate cells (HSCs). Indeed, HSCs are able to adopt a myofibroblastic phenotype that is responsible for the development of fibrosis, an advanced stage of chronic liver diseases characterized by an alteration of the extracellular matrix surrounding hepatocytes.

Our team studies the molecular mechanisms at play in diseased livers that underlie alterations in hepatocyte and HSC phenotypes and activities. Specifically, we investigate how alterations in gene expression occur in these cells and whether these can be corrected to restore normal cellular functions. Finally, given that liver cells communicate directly with each other, we are also studying how changes in gene expression translate into changes in the intercellular dialogue in diseased livers.

Through our work, we hope to contribute to a better understanding of the molecular mechanisms underlying alterations to liver functions with the aim to identify potential new strategies to treat liver diseases.

Keywords

Cell identity; functional genomic; MASLD; nuclear receptor; transcriptional regulation; liver failure; liver fibrosis

Technological approaches

Multi-omics (transcriptomics, cistromics, epigenomics, proteomics...)

Bioinformatical data mining (bulk and scRNAseq, ChIPseq etc)

Mouse models of liver diseases and fibrosis

Primary mouse liver cells and liver slices