First published April 1, 2005 - More info
Liver fibrosis is the excessive accumulation of extracellular matrix proteins including collagen that occurs in most types of chronic liver diseases. Advanced liver fibrosis results in cirrhosis, liver failure, and portal hypertension and often requires liver transplantation. Our knowledge of the cellular and molecular mechanisms of liver fibrosis has greatly advanced. Activated hepatic stellate cells, portal fibroblasts, and myofibroblasts of bone marrow origin have been identified as major collagen-producing cells in the injured liver. These cells are activated by fibrogenic cytokines such as TGF-β1, angiotensin II, and leptin. Reversibility of advanced liver fibrosis in patients has been recently documented, which has stimulated researchers to develop antifibrotic drugs. Emerging antifibrotic therapies are aimed at inhibiting the accumulation of fibrogenic cells and/or preventing the deposition of extracellular matrix proteins. Although many therapeutic interventions are effective in experimental models of liver fibrosis, their efficacy and safety in humans is unknown. This review summarizes recent progress in the study of the pathogenesis and diagnosis of liver fibrosis and discusses current antifibrotic strategies.
Ramón Bataller, David A. Brenner
Original citation: J. Clin. Invest.115:209–218(2005). doi:10.1172/JCI24282
Citation for this corrigendum: J. Clin. Invest.115:1100 (2005). doi:10.1172/JCI24282C1
PPARg agonists but not PPAR antagonists, as listed in Table 2, have shown inhibitory effects on HSCs and antifibrotic effects in animal models with liver fibrosis and patients with NASH.
The authors regret the error.