Targeting collagen expression in alcoholic liver disease

• Published in: World journal of gastroenterology : WJG 2011-05, Vol.17 (20), p.2473-2481
• Main Authors: Thompson, Kyle J, McKillop, Iain H, Schrum, Laura W
• Format: Article
• Language: English
• Subjects: ALD; Animals; Antioxidants - therapeutic use; Collagen Type I - metabolism; Disease Models, Animal; Humans; Liver Cirrhosis - drug therapy; Liver Cirrhosis - metabolism; Liver Diseases, Alcoholic - drug therapy; Liver Diseases, Alcoholic - metabolism; MicroRNAs - therapeutic use; Topic Highlight; 发达国家; 细胞外基质; 肝病; 肝纤维化; 肝脏疾病; 胶原蛋白; 酒精性
• ISSN: 1007-9327; 2219-2840
• DOI: 10.3748/wjg.v17.i20.2473

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.