Open AccessTargeting collagen expression in alcoholic liver disease
Author(s) -
Kyle J. Thompson,
Iain H. McKillop,
Laura W. Schrum
Publication year - 2011
Publication title -
world journal of gastroenterology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.427
H-Index - 155
eISSN - 2219-2840
pISSN - 1007-9327
DOI - 10.3748/wjg.v17.i20.2473
Subject(s) - alcoholic liver disease , cirrhosis , extracellular matrix , fibrosis , medicine , hepatocellular carcinoma , chronic liver disease , pathology , liver disease , hepatic stellate cell , liver injury , type iv collagen , type i collagen , biology , laminin , microbiology and biotechnology
Alcoholic liver disease (ALD) is a leading cause of liver disease and liver-related deaths globally, particularly in developed nations. Liver fibrosis is a consequence of ALD and other chronic liver insults, which can progress to cirrhosis and hepatocellular carcinoma if left untreated. Liver fibrosis is characterized by accumulation of excess extracellular matrix components, including type I collagen, which disrupts liver microcirculation and leads to injury. To date, there is no therapy for the treatment of liver fibrosis; thus treatments that either prevent the accumulation of type I collagen or hasten its degradation are desirable. The focus of this review is to examine the regulation of type I collagen in fibrogenic cells of the liver and to discuss current advances in therapeutics to eliminate excessive collagen deposition.