Adipokines and liver fibrosis

Liver fibrosis involves differ- ent cell types, and should be regarded as a "wound healing" response that occurres in conditions of chronic liver injury and is charac- terized by inflammation, activation of matrix- producing cells, matrix deposition and remod- eling, and epithelial cell regeneration or an at- tempt thereof. Liver damage may be caused by several agents or conditions, resulting in differ- ent degrees and types of tissue inflammation and in activation of matrix-produc ing cells, such as the hepatic stellate cells (HSC). HSC undergo a phenotypic transition (known as "ac- tivation") to myofibroblast-like cells that syn- thesize different extracellular matrix compo- nents. Obesity is associated with the development of NASH, and has been indicated as an inde- pendent factor for the progression to fibrosis. In liver diseases, the biologic actions of the adipokines, such as leptin, adiponectin and re- sistin, released by adipocytes or locally pro- duced by liver and/or inflammatory cells, may contribute to clarify the mechanisms of pro- gression in NASH. The clinical and experimen- tal findings accumulating on this class of mole- cules could represent the basis to devise a bet- ter management strategy for the patients with chronic liver disease.