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Reversal of hepatic fibrosis: pathophysiological basis of antifibrotic therapies

Department of Internal Medicine; Division of Gastroenterology, King Fahad University Hospital, Al-Khobar, Saudi Arabia; Dipartimento di Medicina Interna Center for Research, High Education and Transfer, Università degli Studi di Firenze, Florence, Italy Correspondence; College of Medicine, Department of Internal Medicine, Division of Gastroenterology, University of Dammam; King Fahad Hospital, PO Box 40149, Saudi Arabia
Hepatic Medicine: Evidence and Research 01/2011; 3:69-80. DOI: 10.2147/HMER.S9051

ABSTRACT Chronic liver injuries of different etiologies eventually lead to fibrosis, a scarring process associated with increased and altered deposition of extracellular matrix in the liver. Progression of fibrosis has a major worldwide clinical impact due to the high number of patients affected by chronic liver disease which can lead to severe complications, expensive treatment, a possible need for liver transplantation, and death. Liver fibrogenesis is characterized by activation of hepatic stellate cells and other extracellular matrix producing cells. Liver fibrosis may regress following specific therapeutic interventions. Other than removing agents causing chronic liver damage, no antifibrotic drug is currently available in clinical practice. The extent of liver fibrosis is variable between individuals, even after controlling for exogenous factors. Thus, host genetic factors are considered to play an important role in the process of liver scarring. Until recently it was believed that this process was irreversible. However, emerging experimental and clinical evidence is starting to show that even cirrhosis in its early stages is potentially reversible.

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Jun 5, 2014