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Abstract
Liver fibrosis represents a wound healing response which is caused by a variety of stimuli and poses a significant health problem worldwide. Liver fibrosis is one of the leading causes of morbidity and mortality worldwide, but very limited therapeutic options are currently available for this condition.Currently, no acceptable therapeutic strategies exist, other than removal of the fibrogenic stimulus, to treat this potentially devastating disease. For advanced end-stage liver fibrosis (cirrhosis) the only therapeutic option is liver transplantation, which poses significant risk to the patient. Therefore, a great deal of research is being pursued to understand the molecular basis for the development and progression of liver fibrosis in order to identify effective therapeutic approaches. Fibrosis is characterized by an increase in the synthesis and deposition of collagen. Indisputable evidence now exists that HSCs play a central role in hepatic fibrogenesis secondary to virtually all types of liver injury. In spite of the different forms of initial insult to the liver, affecting different cell populations through diverse mechanisms, and inducing the release of various combinations of mediators, activation of stellate cells represents the unifying pathophysiologic consequence of all forms of chronic liver injury: the convergence point of multiple pathways that ultimately lead to liver fibrosis.
the HSCs functions not only in liver injury, but also in hepatic development, regeneration, xenobiotic responses, intermediary metabolism, and immunoregulation. Among the most exciting prospects is that stellate cells are essential for hepatic progenitor cell amplification and differentiation.