Liver fibrosis and therapeutic strategies: the goal for improving metabolism.
OBJECTIVE
This review summarizes the current state of knowledge on non-alcoholic fatty liver disease (NAFLD) and the hepatitis C virus (HCV)-associated liver fibrosis, and provides insight into the role of dysmetabolism in hepatic fibrogenesis. Clinical relevance of drugs correcting these metabolic disturbances in the reversion of liver fibrosis will also be discussed.


RESULTS
Liver fibrosis affects more than ten millions of people worldwide and may lead to cirrhosis, liver failure, and death. Recent epidemiological data indicate that the incidence of liver fibrosis is expected to triple during the next 10 to 15 years as a result of the HCV infection and NAFLD escalation. In accordance with the modern view of liver fibrogenesis, the pathways involved in the pathogenesis of hepatic fibrosis appear to be broadly similar regardless of the etiology.


CONCLUSIONS
Some features of metabolic syndrome, including obesity, insulin resistance, and type 2 diabetes represent a strong risk factor in development and progression of hepatic fibrosis. However, whatever the cause, fibrosis culminates in cirrhosis and results in liver failure, thus, a potent anti-fibrotic therapy is urgently needed to reverse scarring and eliminate progression to cirrhosis.
Balsano
Clara
C
Laboratory of Molecular Virology and Oncology, A Cesalpino Foundation, University of Rome, Rome, Italy. clara.balsano@uniroma1.it
Alisi
Anna
A
Nobili
Valerio
V
D000818:Animals; D005234:Fatty Liver / Q000150:complications; D006526:Hepatitis C / Q000150:complications; D006801:Humans; D008103:Liver Cirrhosis / Q000209:etiology / Q000378:metabolism* / Q000628:therapy*; D008954:Models, Biological; D012307:Risk Factors