Targeting collagen expression in alcoholic liver disease

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 un-treated.Liver fibrosis is characterized by accumulation of excess extracellular matrix components,including typeⅠcollagen,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 typeⅠcollagen or hasten its degradation are desirable.The focus of this review is to examine the regulation of typeⅠcollagen in fibrogenic cells of the liver and to discuss current advances in therapeutics to eliminate excessive collagen deposition.

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.