Based on our long-standing expertise in metabolic diseases, we focus our efforts to make significant progress in research related to liver diseases. Amongst these diseases, our major working axis are devoted to NASH.
A particular focus of our research is the identification of new products capable of halting the fibrotic process that develops during the evolution of chronic liver diseases and significantly contributes to their worsening.
The liver is a vital organ that plays an essential role in detoxification and nutrient storage. Because of its key roles in glucose and lipid metabolism, several liver diseases are associated with alterations in metabolic activities.
A dysfunctional liver can lead to serious illnesses and jeopardize the vital prognosis.
There are many types of liver diseases, with multiple origins including viral infection, metabolic dysfunction, autoimmunity, alcohol, or toxins. In their most advanced stages, liver diseases are associated with serious complications (encephalopathy, esophageal hemorrhage, ascites) that can ultimately require liver transplantation, and even be life-threatening.
Hepatitis are characterized by a destruction of liver cells called hepatocytes. The destruction of hepatocytes is progressive in chronic hepatitis but can proceed very rapidly in fulminant hepatitis.
Chronic hepatitis is associated with a persistent inflammatory reaction which is accompanied by a scarring process leading to a progressive accumulation of extracellular matrix (cirrhosis). In the late stage, when the fibrosis is widespread and the liver is no more able to assume its function, decompensated cirrhosis occurs. At present, there is no existing treatment for reducing fibrosis in chronic hepatitis.
Hepatic fibrosis leads to significant morbidity and mortality in chronic liver diseases of different origins, such as viral hepatitis, NASH, alcoholic steatosis, acute liver failure, and others.
The most common types are hepatitis A, B and C. Chronic hepatitis C infection is the leading cause for liver transplantation in Western countries, although this tends to be reduced with the use of antiviral agents that are becoming more and more efficient.
Nonalcoholic steatohepatitis (NASH)
The prevalence of NASH is a consequence of the world obesity epidemic, and as a result, there is a growing number of cirrhosis, hepatic insufficiency, liver transplantation, and mortality. To date, there is no treatment for NASH.
Alcoholic hepatitis and cirrhosis
Well-known pathologies that are caused by an overconsumption of alcohol over a long period of time. These remain the major causes of hepatic insufficiency and liver cancer.
Hepatitis or cirrhosis associated with bile ducts diseases
These rare, slowly progressive diseases with a high morbidity, affect the intra- or extrahepatic bile ducts. 2 major types have been identified: Primary Biliary Cirrhosis (PBC) and Primary Sclerosing Cholangitis (PSC). PBC is currently insufficiently managed and there is no actual treatment for PSC.
Other forms of hepatitis have a genetic origin (such as Wilson’s disease, or Alpha1-antitrypsine deficiency) or result from an uncontrolled immune system (autoimmune hepatitis).
Fulminant hepatitis or acute liver failure
Acute liver failure is characterized by sudden and massive liver injuries in patients without previous history of chronic hepatitis. Many of these result from drug intoxication, the most frequent case being drug-induced hepatitis with overdosage of paracetamol. Fulminant hepatitis is difficult to control and necessitates emergency care and in certain cases, liver transplantation may be needed within a short delay.
A primary liver cancer may occur in patients with advanced cirrhosis or chronic hepatitis caused by a virus such as hepatitis B.
Primary liver cancer is rare in comparison to liver cancer derived from metastasis (in particular, colorectal cancer). Although the surgical resection of cancerous nodules is often performed, there is a medical need for novel anticancer agents and most notably, for new drugs destined to favor hepatic regeneration after resection.