Hepatic fibrosis.
OBJECTIVE
This review will summarize the most significant work that contributed to the understanding of liver fibrosis progression and resolution, which in turn has yielded new areas of therapeutic targeting.


RESULTS
Liver fibrosis is the result of an imbalance between production and dissolution of extracellular matrix. Stellate cells, portal myofibroblasts, and bone marrow derived cells converge in a complex interaction with hepatocytes and immune cells to provoke scarring in response to liver injury. Uncovering the specific effects of growth factors on these cells, defining the interaction of different cell population during liver fibrosis and characterizing the genetic determinants of fibrosis progression will enable the discovery of new therapeutic approaches.


CONCLUSIONS
The outcome of improved understanding of liver fibrosis process, especially the regulation and activation of stellate cells, is reflected in the development of new therapeutic strategies, which are validated in animal models.
Jiao
Jingjing
J
Division of Liver Diseases, Mount Sinai School of Medicine, New York, New York 10029-6574, USA.
Friedman
Scott L
SL
Aloman
Costica
C
D020533:Angiogenesis Inhibitors / Q000627:therapeutic use*; D000818:Animals; D018450:Disease Progression; D016326:Extracellular Matrix Proteins / Q000378:metabolism*; D055166:Hepatic Stellate Cells / Q000473:pathology*; D006801:Humans; D008103:Liver Cirrhosis / Q000378:metabolism / Q000473:pathology / Q000628:therapy; D016031:Liver Transplantation / Q000379:methods*; D011379:Prognosis
D020533:Angiogenesis Inhibitors; D016326:Extracellular Matrix Proteins